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Minipress (Prazosin)

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Minipress is an effective strong preparation which is taken in treatment of hypertension diseases. Minipress is also helpful in treatment of male prostate enlargement symptoms, congestive heart failure, Raynaud's disease. Minipress acts as anti-hypertension remedy.

Other names for this medication:

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Lisinopril, Amlodipine, Norvasc, Benicar, Metoprolol, Hydrochlorothiazide, Avapro, Losartan


Also known as:  Prazosin.


Minipress is created by pharmacy specialists to combat hypertension disease. Target of Minipress is to control level of blood pressure.

Minipress acts as anti-hypertension remedy. Minipress operates by reducing blood pressure.

Minipress is also known as Prazosin, Prazopress, Vasoflex, Hypovase.

Minipress is alpha blocker.

Generic name of Minipress is Prazosin (oral).

Brand name of Minipress is Minipress.


You should take it by mouth with water.

It is better to take Minipress 2-3 times a day at the same time with meals or milk.

It is better to start the first Minipress dose when are going to bed.

If you want to achieve most effective results do not stop taking Minipress suddenly.


If you overdose Minipress and you don't feel good you should visit your doctor or health care provider immediately. Symptoms of Minipress overdosage: feeling lightheaded, rash, weakness, troublesome breathing, pruritus, swelling.


Store at room temperature between 15 and 30 degrees C (59 and 86 degrees F) away from moisture, light and heat. Keep container tightly closed. Throw away any unused medicine after the expiration date. Keep out of the reach of children in a container that small children cannot open.

Side effects

The most common side effects associated with Minipress are:

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Side effect occurrence does not only depend on medication you are taking, but also on your overall health and other factors.


Do not take Minipress if you are allergic to Minipress components.

Be careful with Minipress if you're pregnant or you plan to have a baby, or you are a nursing mother.

Be careful with Minipress if you are taking any prescription or nonprescription medicine, herbal preparation, or dietary supplement.

Be careful with Minipress if you have allergies to medicines, foods, or other substances.

Be careful with Minipress if you have liver or kidney disease, heart failure, low blood pressure, narcolepsy, prostate cancer.

Be careful with Minipress if you take muscle relaxants as carisoprodol; anti-anxiety drugs as diazepam; anti-seizure drugs as carbamazepine; tranquilizers; sleep medicines as sedatives; antihistamines as diphenhydramine; verapamil; psychiatric medicines as tricyclic antidepressants (amitriptyline), phenothiazines (chlorpromazine); sexual function problems drugs as vardenafil, sildenafil, tadalafil; narcotic pain relievers as codeine; beta blockers as metoprolol, propranolol, atenolol.

Avoid machine driving.

Use Minipress with great care in case you want to undergo an operation (dental or any other).

Avoid alcohol.

Minipress can be not safety for elderly people.

Try to be careful with sunbeams. Minipress makes skin sensitive to sunlight. Protect skin from the sun.

Do not stop taking Minipress suddenly.

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The action of dexmedetomidine on rat locus coeruleus neurones was examined using intracellular recordings from the in vitro brain slice preparation. Concentrations of dexmedetomidine from 1 to 1000 nM were tested. At 30 nM, dexmedetomidine produced complete inhibition of firing of all neurones tested (n = 21); this was associated with a 13 mV hyperpolarization (range 2.2-29.7 mV, n = 21) and a 27% reduction in input resistance (range 11.1-46.2%, n = 17). The dexmedetomidine responses reached a plateau phase between 100 and 1000 nM. Based on single-cell recordings, the hyperpolarizing potency of dexmedetomidine was found to be 6 times greater than that of clonidine (n = 10). The reversal potential for the dexmedetomidine-induced hyperpolarization was -106.9 +/- 1.7 mV (n = 9), a value similar to the K+ equilibrium potential; hyperpolarization was blocked by both CsCl and BaCl2. The effect of dexmedetomidine was antagonized by yohimbine, with a dissociation equilibrium constant of 30 nM. In contrast, prazosin, the alpha 1-, alpha 2B- and alpha 2C-adrenoceptor subtype-preferring ligand, did not inhibit the dexmedetomidine effect. Our results also show that low concentrations of oxymetazoline (10-300 nM), an alpha 2A-adrenoceptor subtype-selective drug, cause profound inhibition of neuronal activity in the locus coeruleus. These data therefore suggest that dexmedetomidine binds to alpha 2A-adrenoceptors on the cell membrane of neurones of the locus coeruleus and that this leads to opening of the inwardly rectifying K+ channels, resulting in the observed hyperpolarization of the membrane.

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Adrenergic stimulation of the heart leads to activation of the phospholipase D signal transduction pathway with formation of the intracellular second messengers phosphatidic acid and diacylglycerol, which may play a role in the development of myocardial hypertrophy by activating mitogen-activated protein kinases and protein kinase C. So far, the adrenergic receptor subtypes mediating activation of cardiac phospholipase D are not known.

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The numbers of fully adherent (20/40 versus 21/45), partially nonadherent (13/40 versus 20/45), or completely nonadherent patients (7/40 versus 4/45) to antihypertensive treatment were not different in the renal denervation and the control groups, respectively (P=0.3605). The difference in the change in daytime ambulatory systolic blood pressure from baseline to 6 months between the 2 groups was -6.7 mm Hg (P=0.0461) in fully adherent and -7.8 mm Hg (P=0.0996) in nonadherent (partially nonadherent plus completely nonadherent) patients. The between-patient variability of daytime ambulatory systolic blood pressure was greater for nonadherent than for fully adherent patients.

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Using a number of agonist and antagonist compounds, we attempted to characterize the responses and receptors involved in the effects of 5-hydroxytryptamine (5-HT) in the in situ autoperfused rat kidney. An intra-arterial (i.a.) bolus injection of 5-HT (0.0125 to 0.1 microg/kg) increased renal perfusion pressure in a dose-dependent way but did not change the systemic blood pressure. The 5-HT2 receptor agonist, (1-(3-chlorophenyl) piperazine), m-CPP, caused a local vasoconstrictor effect in the autoperfused rat kidney. An intra-arterial injection of 5-carboxamidotryptamine, 5-CT and 1-(m-chlorophenyl)-biguanide (m-CPBG) did not modify the renal perfusion pressure. The vasoconstrictor effect elicited by 5-HT and m-CPP was significantly decreased by ritanserin, enalapril and losartan but was not modified by prazosin, propranolol or indomethacin pretreatment. Our data suggest that the vasoconstrictor serotonergic response induced in the in situ autoperfused rat kidney is mediated through angiotensin II activation by a local 5-HT2 receptor mechanism.

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The concept of a tonic drive activating respiratory muscle in wakefulness but not sleep has been an important and enduring notion in respiratory medicine, not least because it is useful in modeling sleep effects on breathing and understanding the pathogenesis of sleep-related breathing disorders such as obstructive sleep apnea. However, a neurotransmitter substrate mediating respiratory muscle activation across sleep-wake states has not been identified.

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Ten healthy subjects were investigated in a randomized, single-blind, three-way cross-over design and received a single dose of 0.4 mg tamsulosin, 5 mg terazosin or placebo on 3 study days at least 1 week apart. Before and 1, 3, 5, 7, 10 and 23.5 h after drug intake, alterations of diastolic blood pressure and other haemodynamic parameters in response to a graded infusion of the alpha1-adrenoceptor agonist phenylephrine were determined non-invasively.

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Controlled clinical studies have demonstrated that blockade of alpha 1-adrenergic receptors relaxes prostatic muscle tone and decreases the symptoms of benign prostatic hyperplasia (BPH). Doxazosin, a once-daily quinazoline derivative and postsynaptic alpha 1-adrenoceptor antagonist, proven as treatment for hypertension, was evaluated in the treatment of BPH in dosages of 1-16 mg. 456 BPH patients (287 doxazosin-treated and 169 placebo-treated) were evaluated for efficacy and safety in five double-blind, placebo-controlled clinical studies. Doxazosin treatment resulted in improvements in both urodynamic and symptomatic parameters associated with BPH. Efficacy was only assessed in 1, 2 and 4 mg. Adverse experiences were reported in 127 (44.3%) of the patients treated with doxazosin and in 49 (29%) of the patients treated with placebo. Fifteen (5.2%) doxazosin patients and 4 (2.4%) placebo patients withdrew from the studies due to adverse effects. Results from these five clinical trials demonstrate doxazosin is effective and safe and well tolerated in both normotensive and hypertensive patients with BPH.

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Using constant infusion technique and a water-loading procedure, we investigated renal hemodynamic and excretional variables in 15 essential hypertensive patients [diastolic blood pressure (DBP) 102 +/- 10 mm Hg] after 3 weeks of placebo and after 16 weeks of treatment with a postjunctional alpha 1-adrenoceptor-antagonist, doxazosin (1-16 mg) once daily. A minor decrease in supine DBP (p less than 0.05) but no significant changes in systolic BP (SBP) and heart rate (HR) were observed. No significant changes were noted in glomerular filtration rate (GFR), renal plasma flow (RPF), and renal vascular resistance (RVR). The mean renal excretion rate of sodium, potassium, uric acid, and albumin for the entire group was unaffected by the treatment, but the individual changes in sodium clearance correlated significantly with changes in mean BP (r = 0.64, n = 15, p less than 0.05). Six patients showed an increase in sodium excretion after treatment, whereas nine showed a decrease. No decrease in mean body weight was noted, but the BP reduction after 5 months of treatment correlated significantly with the changes in body weight (r = 0.62, n = 15, p less than 0.01). The results indicate that long-term treatment with doxazosin had no deleterious effect on renal function, but the effects on BP were rather modest. The individual BP response is probably determined by the degree of fluid retention even if an intact pressure-natriuresis relationship could still be demonstrated during chronic therapy.

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After chronic treatment with imipramine (20 mg/kg, i.p., twice daily for 14 days) the pressor dose-response curves to phenylephrine, methoxamine and cirazoline (alpha 1-adrenoceptor agonists) significantly shifted to the left with decreased PD50 values in pithed rats; however, the dose-response curve to Sgd 101/75, a selective alpha 1-adrenoceptor agonist was not affected. On the other hand, the alpha 2-adrenoceptor agonists such as B-HT 920, xylazine and clonidine produced a rightward shift for both the pressor (increased PD50) and cardioinhibition (increased ID50) dose-response curves in these rats. These results required treatment with imipramine over 2 weeks. Chronic treatment with imipramine has reduced the antagonism by prazosin of the pressor effect of phenylephrine when compared with the dose-ratios between the 2 groups. On the contrary, the antagonism by piperoxan of the cardioinhibitory effect of B-HT 920 was rather enhanced by the treatment, but that of the pressor effect of B-HT 920 was little changed. In cerebrocortical membrane fractions obtained from rats pretreated with imipramine, Ki of phenylephrine to displace [3H]prazosin was decreased, whereas that of clonidine and yohimbine to displace [3H]yohimbine was increased. In conclusion, it is demonstrated that after chronic imipramine treatment the peripheral alpha 2-adrenoceptors (both presynaptic and postsynaptic sites) as well as central alpha 2-adrenoceptors respond with a decreased sensitivity to the alpha 2-adrenoceptor agonists, and moreover, this treatment produces an increased sensitivity of the central and peripheral alpha 1-adrenoceptors to the alpha 1-adrenoceptor full agonists.

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Methamphetamine (METH) is a psychostimulant that damages nigrostriatal dopaminergic terminals, primarily by enhancing dopamine and glutamate release. α₁-adrenergic receptor (AR) subtype involved in METH-induced neurotoxicity in rats was investigated using selective α₁-AR antagonists. METH neurotoxicity was evaluated by (1) measuring body temperature; (2) determining tyrosine hydroxylase (TH) immunoreactivity levels; (3) examining levels of dopamine and its metabolites; and (4) assessing glial fibrillary acidic protein (GFAP) and microglial immunoreactivity in the striatum. METH caused a decrease in dopamine and TH levels and induced hyperthermia which is an exacerbating factor of METH neurotoxicity. Concurrently, METH increased GFAP expression and the number of activated microglia. Pretreatment with prazosin, a nonselective α₁-AR antagonist, completely abolished METH-induced decrease in both dopamine and TH and caused a partial reduction in hyperthermia. Prazosin also prevented METH-induced increase in both GFAP expression and the number of activated microglia. In vivo microdialysis analysis revealed that prazosin, however, does not alter the METH-induced dopamine release in the striatum. The neuroprotective effects of prazosin could be mimicked by a selective α(1D) antagonist, BMY 7378, but not by selective α(1A) or α(1B) antagonists. These results suggest that the α(1D)-AR is involved in METH-induced hyperthermia and neurotoxicity in rats.

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Major variations in the consumption of cardiovascular drugs between healthcare areas, together with discreet variations in price mean there are big differences in pharmaceutical expenditure from one population to another.

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Ventricular myocytes isolated from the hypertrophied hearts of thyrotoxic adult rats have an increase in mean protein content per myocyte (6.3 +/- 0.2 vs. 4.4 +/- 0.2 ng) compared with euthyroid cells. Viability and adenine nucleotide profiles are similar in both populations, but NAD content of the hyperthyroid myocytes is depressed (4.9 +/- 0.2 vs. 5.5 +/- 0.2 nmol/mg for controls) and UTP is higher (1.2 +/- 0.09 vs. 0.9 +/- 0.04 nmol/mg). Binding of (-)-[125I]iodocyanopindolol to intact hyperthyroid myocytes is increased by 42% compared with controls, with no change in the dissociation constant (Kd). This elevation in beta-receptor number is correlated to enhanced beta-agonist-induced adenosine 3',5'-cyclic monophosphate (cAMP) production. The half-maximal effective concentration (EC50) for the euthyroid isoproterenol dose-response curve is 2.14 x 10(-7) M but is decreased to 2.51 x 10(-8) M in hyperthyroid cardiac cells. Basal adenylate cyclase activity is apparently not affected by thyroid hormones, since basal cAMP levels for both groups are identical (5 pmol/mg) and both rise roughly twofold in the presence of a phosphodiesterase inhibitor. Forskolin-induced cAMP production and cAMP-specific phosphodiesterase activity are similar as well. In contrast to beta-adrenergic response, there are no significant differences in alpha 1-antagonist [3H]prazosin binding parameters between hyperthyroid and euthyroid cardiomyocytes.

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Human prostatic stromal cells were isolated from prostatectomy and cystoprostatectomy specimens. The cells were cultured in a selective medium supplemented with growth factors and steroid hormones. The culture flasks were coated with a viscous agent to allow cell contraction. Contractions were visualized by means of a cell-culture microscope fitted with a time-lapse video system. For quantitative analysis, the percentage of contracting cells was evaluated.

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The effects of excitatory amino acid agonists on [3H]inositol phosphates (InsPs) levels have been examined in rabbit retinal tissues under basal conditions and after agonist stimulation. Quisqualate (QA) is the most effective excitatory amino acid agonist at stimulating InsPs accumulation with an EC50 value of 0.1 microM. The responses for maximally effective concentrations of QA with either ibotenate or kainate were not additive, which suggested that all the excitatory amino acid agonists which stimulate InsPs accumulation (quisqualate, kainate, NMDA, glutamate, ibotenate, aspartate) have a common site of action. None of the following antagonists: DL-2-amino-5-phosphonovalerate (APV), DL-2-amino-4-phosphonobutyrate (APB) and glutamate dimethyl ester (GDEE), prazosin, ketanserin or atropine influenced the excitatory amino agonist stimulation of InsPs. These data suggest the presence of a specific QA-receptor subtype in the retina. QA, and to a lesser extent other excitatory amino acid agonists, were also effective in stimulating InsPs accumulation and the mobilization of internal calcium levels in 3-5-day-old retinal cultures but not in the older cultures (25-30 days old), which lack neurones but contain Müller cells. The QA receptor subtypes linked to InsPs accumulation in the retina are therefore present on neurones. Kainate and NMDA had a weak inhibitory action on the effect of the carbachol-induced stimulation of InsPs at 50 microM. The NMDA action was abolished by APV, whereas this antagonist had no effect on the action of kainate.(ABSTRACT TRUNCATED AT 250 WORDS)

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Both treatment methods seemes to be effective in detrusor-sphincter discoordination. Selective alpha1-blockers alone are more effective than training and rehabilitation exercises.

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To examine the effect of adrenergic blockade on daily rhythms of rectal body temperature (T(b)), urine production rate, and melatonin (MEL; measured as urinary 6-sulfatoxymelatonin; 6-SMT), social voles Microtus socialis received a single intra-peritoneal injection of either prazosin (PRAZ, 1 mg/kg) or propranolol (PROP, 4.5 mg/kg); alpha- and beta-adrenergic blocking agents respectively, 1 h prior to scotophase onset (light/dark, 12L:12D; lights on 07:00 h). Both blockers caused significant decrease in T(b) values mainly during scotophase. Nocturnal urine production rates were higher for M. socialis treated with the drugs compared with controls. Overall, urine production rates were systematically higher in PROP-voles over the 24 h period when compared with PRAZ-voles; however these differences were not statistically significant. Interestingly, PROP caused significant elevation in urinary 6-SMT at the second half of the dark phase, whereas PRAZ had no effects. These data suggest that the mechanisms regulating MEL synthesis and thermoregulatory responses in M. socialis are different from those described in other rodents' species. Importantly, the data also suggest that the beta-blockade-induced elevation in MEL levels may be directly associated with increased urination in M. socialis.

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We attempted to determine which monoamine receptor subtypes are predominantly involved in antidepressant-induced antinociception. Antinociceptive effects were evaluated by using formalin tests with rats. Antidepressants acting as potent inhibitors of norepinephrine reuptake (nisoxetine, nortriptyline, and maprotiline) or inhibiting reuptake of both norepinephrine and serotonin (5-HT) (imipramine and milnacipran) induced dose-dependent antinociception. Simultaneous intraperitoneal administration of antidepressants and either prazosin (alpha(1) antagonist) or ketanserin (5-HT(2) antagonist) significantly antagonized antinociceptive effects. Fluvoxamine (selective serotonin reuptake inhibitor) induced antinociception less potently than other antidepressants and was significantly antagonized by ketanserin, but not prazosin. Ondansetron (5-HT(3) antagonist) significantly antagonized antinociception by 10 mg/kg of imipramine. In contrast, SDZ-205,557 (5-HT(4) antagonist) markedly enhanced antinociception by small-dose (2.5 mg/kg) imipramine. Imipramine-induced antinociception was significantly antagonized by intracerebroventricular administration of prazosin or ketanserin, but not by yohimbine (alpha(2) antagonist) or ondansetron, and was significantly enhanced by intracerebroventricularly administered SDZ-205,557. These findings suggest that alpha(1) adrenoceptors and 5-HT(2) receptors in the brain are involved in antidepressant-induced antinociception. In addition, the results suggested functional interactions between noradrenergic and serotonergic neurons as mechanisms for antidepressant-induced antinociception.

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We have recently reported that the responsiveness of adrenoceptors is decreased with aging in rat ventricular myocardium. Thus, the current study determined aging-dependent changes in: (a) characteristics of myocardial G proteins as determined by Western blot analysis; (b) steady-state levels of G protein mRNA as determined by Northern blot analysis; and (c) the intropic response to isoproterenol, a beta-adrenoceptor agonist. Cardiac preparations were isolated from male Wistar rats of 6 (adult) and 24 (old) months old. Compared with adults, aging decreased the combined level of the three Gs alpha subunits (45, 47 and 52 kDa) by a total of 23% in ventricular membrane preparations. In contrast, levels of Gi alpha (40/41 kDa), Gq alpha (42 kDa), Go alpha (39 kDa) and G common beta (35/36 kDa) immunoreactivity were not affected by aging in the same membrane preparations. In ventricular myocardium, steady-state levels of Gs alpha mRNA (1.9 kb) decreased by 20-28% between 6 and 24 months of age with no change in Gi alpha mRNA (2.4 kb). An aging-associated decline in beta-adrenergic stimulation was observed in the maximum positive inotropic effect elicited by isoproterenol in the presence of prazosin in left papillary muscles, with no change in ED50 values. These results suggest that age-related changes in cardiac excitation and contraction coupling following beta-adrenoceptor stimulation are mediated, at least in part, by Gs alpha protein dysfunction.

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By the introduction of the vasodilators into the therapy of the cardiac insufficiency particularly by the application of angiotensin-converting-enzyme (ACE) inhibitors advance could be obtained with regard the peripheral resistance which is always made evident as a sequel of the vasoconstriction in severe cardiac insufficiency the application of vasodilating substances (venous or arterial) leads to a relief of the heart with increase of the cardiac output, decrease of the congestion symptoms and partly amelioration of the exercise tolerance. Whereas all vasodilating substances show these effects in the acute experiment, in the long-term application due to the tolerance development no significant haemodynamic and clinical amelioration is to be made evident any more, with the exception of the ACE-inhibitors. Only the combination of nitrates and hydralazine showed favourable results with regard to the survival time. The therapy with ACE-inhibitors is, when they is used in an expert way and aimed, the hitherto most conducive one to success which has only slight side-effects. Because of the present knowledge all patients with a cardiac insufficiency of the degrees of severity III and IV, perhaps already beginning with degree of severity II, should, in addition to glycosides and diuretics, be treatment with ACE-inhibitors, so far as no contraindication or intolerability are present. Otherwise an experiment with nitrates plus hydralazine is justified.

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The contributions of subtypes of alpha-adrenoceptor to contraction induced by agonists were studied in smooth muscles of isolated rat pulmonary arteries. The results showed that the antagonizing effects of prazosin on the contraction induced by norepinephrine (NE) or phenylephrine (Phe) were more potent than those of yohimbine. The effect of prazosin against Phe was more potent than against NE, and yohimbine was just the reverse. Preincubation of preparations with chlorethylclonidine (CEC) 50 mumol.L-1, after which only alpha 1A adrenoceptors were left, reduced the vascular contraction induced by NE to 36% of the control (P < 0.01). While in the presence of nifedipine 10 mumol.L-1, during which only the responses of alpha 1B adrenoceptors were left, the contraction was weakened to 70% (P < 0.05). The pKA values of alpha 1A subtype (3.37 +/- 0.34) were smaller than those of alpha 1B (6.64 +/- 0.40, P < 0.01). But the values of KA/EC50 were much higher in alpha 1A than those in alpha 1B. The results suggest that in smooth muscle of rat pulmonary artery both alpha 1 and alpha 2 adrenoceptors exist, but alpha 1 is superior functionally. Both subtypes of alpha 1 adrenoceptor are involved in the contraction induced by NE. Compared with alpha 1B subtype, alpha 1A subtype has a lower affinity but a more reserve and a higher efficacy for NE.

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Central catecholamine depletion blocked MDMA-induced hyperthermia and its exacerbation by caffeine. Caffeine provoked a hyperthermic response when the catecholamine releaser d-amphetamine (1 mg x kg(-1)) was combined with the 5-HT releaser D-fenfluramine (5 mg x kg(-1)) or the non-selective dopamine receptor agonist apomorphine (1 mg x kg(-1)) was combined with the 5-HT(2) receptor agonist DOI (2 mg x kg(-1)) but not following either agents alone. Pretreatment with the dopamine D(1) receptor antagonist Schering (SCH) 23390 (1 mg x kg(-1)), the 5-HT(2) receptor antagonist ketanserin (5 mg x kg(-1)) or alpha(1)-adreno- receptor antagonist prazosin (0.2 mg x kg(-1)) blocked MDMA-induced hyperthermia and its exacerbation by caffeine. Co-administration of a combination of MDMA with the PDE-4 inhibitor rolipram (0.025 mg x kg(-1)) and the adenosine A(1/2) receptor antagonist 9-chloro-2-(2-furanyl)-[1,2,4]triazolo[1,5-C]quinazolin-5-amine 15943 (10 mg x kg(-1)) or the A(2A) receptor antagonist SCH 58261 (2 mg x kg(-1)) but not the A(1) receptor antagonist DPCPX (10 mg x kg(-1)) exacerbated MDMA-induced hyperthermia.

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1. In pithed rats, the blood pressure effects of ATP, alpha,beta-methylene ATP (mATP), alpha-adrenoreceptor agonists and of electrical stimulation of the thoracolumbar sympathetic outflow were studied in the absence and presence of mATP, suramin and adrenoreceptor antagonists. 2. ATP elicited an initial rise in mean blood pressure followed by a decrease and a second increase. mATP produced a short-lived increase in blood pressure, whereas equieffective doses of noradrenaline, methoxamine and B-HT 920 (6-allyl-2-amino-5,6,7,8-tetrahydro-4H-thiazolo-(5,4-d)-azepine) produced a more prolonged, biphasic pressor response. 3. In the presence of high doses of prazosin, rauwolscine plus propranolol, the initial vasopressor and the vasodepressor effect to ATP were not affected, whereas the delayed vasopressor response to ATP, the vasopressor response to electrical stimulation and even more so that to noradrenaline were suppressed. 4. Suramin, which by itself produced a short-lived decrease, followed by a persistent increase in blood pressure, decreased the pressor responses to ATP (initial phase), to mATP and to electrical stimulation without affecting the fall and second rise in blood pressure elicited by ATP and the pressor response to noradrenaline. 5. Desensitization of P2x receptors by a low dose of mATP abolished the initial vasopressor response to ATP but failed to affect the subsequent blood pressure effects of ATP as well as the pressor responses to noradrenaline and electrical stimulation. A high dose of mATP, in addition, decreased the vasopressor responses to noradrenaline, methoxamine, B-HT 920 and electrical stimulation; the delayed effects of ATP on blood pressure were not changed. 6. The electrically induced increase in blood pressure subsequent to administration of high doses of prazosin, rauwolscine plus propranolol was diminished by suramin and by the low and high dose of mATP. 7. The present study suggests that under certain circumstances ATP, which, added exogenously, has a triphasic effect on mean blood pressure, contributes to the electrically induced vasopressor response by activation of P2x receptors.

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Previous studies suggest that noradrenaline may regulate serotonergic (5-HT) neurotransmission at the serotonin cell body and noradrenaline nerve terminal. Using microdialysis coupled to HPLC, we investigated the effects of alpha1-adrenoceptor manipulation on extracellular serotonin levels - in the ventral hippocampus, prefrontal cortex, and raphe nuclei - in the presence or absence of the serotonin reuptake inhibitor (SSRI), citalopram. Extracellular 5-HT levels from prefrontal cortex, ventral hippocampus and raphe nuclei were markedly increased following citalopram administration (3.0 mg/kg s.c.). In the prefrontal cortex and ventral hippocampus, local blockade of the alpha1-adrenoceptor (3.0 microM prazosin infusion) significantly decreased this citalopram-induced increase in serotonin, while cirazoline (alpha1-adrenoceptor agonist) and reboxetine (noradrenaline reuptake inhibitor) further increased extracellular serotonin levels when administered systemically (0.02 mg/kg i.p. and 5.0 mg/kg s.c. respectively) or locally infused (10.0 microM and 1.0 microM respectively). Moreover, prazosin pre-infusion into terminal areas prevented the increase in citalopram-induced increase in serotonin levels with systemic cirazoline or reboxetine administration. Prazosin also decreased the citalopram-induced increase in serotonin levels in the raphe nuclei; however no enhancement of the SSRI response was observed with systemic or local administration of cirazoline or reboxetine, suggesting that alpha1-adrenoceptors may already be maximally activated under these conditions. These data provide strong evidence that after acute citalopram administration, the alpha1-adrenoceptor exerts a modulatory role on serotonin levels.

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The purpose of the present investigation was to examine the role of alpha adrenoceptors in the internal anal sphincter (IAS). Studies wer performed on alpha-chloralose anesthetized opossums. Resting pressure in the IAS (IASP) was recorded using low compliant continuously perfused catheters. The effects of the alpha-1 adrenoceptor agonist phenylephrine and alpha-2 adrenoceptor agonist clonidine and their corresponding selective antagonists, prazosin and yohimbine, respectively, were examined on the resting IASP, and on rectal balloon distension (RBD)-mediated IAS relaxation. Phenylephrine caused a rise in the IASP that was blocked by prazosin and not by yohimbine. Phenylephrine had no effect on IAS relaxation caused by RBD. Clonidine on the other hand caused significant suppression of IAS relaxation in response to RBD, but caused minimal changes in the resting IASP. The suppression of IAS relaxation by clonidine was selectively antagonized by yohimbine but not by prazosin. From these studies we conclude that alpha-2 adrenoceptors exert important neuromodulatory influences on rectoanal inhibitory reflex, while alpha-1 adrenoceptors may exert modulatory effects on the resting IAS tone.

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Some of antihypertensives, opiate antagonist and antifungal agent can interfere with sexual function in both men and women. Drug-related effects on sexual function may be difficult to distinguish from the direct action of gonadal function. Clinically well known those agents to have sexual dysfunction were selected and examined the direct effect on rat's testicular steroidogenesis in vitro. Donryu rats were decapitated at 11 weeks old and isolated testes were decapsulated and preincubated with Krebs-Ringer-phosphate buffer (KRP) added with 1 micrograms/flask of LH for 60 min at 37 degrees C. Then, incubation was made with prazosin (1 micrograms), clonidine (5 micrograms), verapamil (10 micrograms), naloxone (5 micrograms) and ketoconazole (150 micrograms), 37 degrees C for 180 min in fresh KRP-buffer, respectively. Steroids were analysed with RIA, and microfluorometry after purification with quantitative thin layer chromatography. Prazosin had a tendency to produce dihydrotestosterone (DHT) indicating a facilitation of 5 alpha-reductase, and clonidine showed a significant production of estradiol (E2) with a slight production of DHT indicating a significant facilitation of aromatase. Verapamil had a action to produce significantly E2 with a slight production of DHT, and naloxone showed a significant production of both DHT and E2. Thus, these two agents showed facilitation of both 5 alpha-reductase and aromatase. Ketoconazole had a significant production of both delta 4-androstenedione (delta 4-A) and E2 while it had a significant inhibition of DHT-production, thus this had a significant production of both aromatase and C17,20-lyase while had a significant inhibitory action of 5 alpha-reductase. These findings indicates that comparatively large doses of central-nervous system depressants are one of the factors that interfere with sexual function, but it is not necessary to have direct action to testicular function, however present study revealed that some of them can cause gonadal damage and consequently progressive loss of libido.

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Oxidative stress can induce cell mutations or proliferation which then can progress to carcinogenesis or remodeling. The same oxidative stress-mediated mechanism could participate in prostate cell proliferation and remodeling present in benign prostatic hyperplasia (BPH). Doxazosin induces prostate epithelial and stromal cell apoptosis through production of transforming growth factor-beta (TGF-beta), but cellular mechanisms are not completely clarified. In 10 prostate samples from BPH untreated patients who underwent TUR, we have assessed the gene and protein expression of: p22(phox) (subunit of NAD(P)H oxidase essential for O(2)(-) production); heme oxygenase-1 (HO-1) (induced by oxidative stress and antiapoptotic); TGF-beta (inhibitor of prostatic epithelial and stromal cell growth); the in vitro effect of doxazosin on expression of these markers.

minipress drug class

This was a randomized, double-blind, double-simulation control study. We equally assigned 60 men diagnosed with BPH of the kidney deficiency and blood stagnation type to an experimental and a control group, the former treated with mesylate doxazosin plus Longbishu Capsule and the latter with mesylate doxazosin plus placebo. We compared the International Prostate Symptom Score (IPSS), quality of life (QOL), Chinese symptom score (CSS), maximal urinary flow rate (Qmax), and prostate volume between the two groups of patients before and after 6 months of medication.

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minipress cost 2015-03-28

The concentrations of TRH in the cerebrospinal fluid (CSF) of the 3rd ventricle were measured with push-pull cannulae in 12 conscious rats. In the basal state the level of TRH in 15 min perfusion samples (210 microliters) were low (2.69 +/- 0.05 pg) and mostly undetectable with the RIA available. However, 70 to 80 min after exposure of the rats to cold (4 degrees C) a short lived but significant rise of TRH was measured in all animals. Post cold peaks amounted to 5.15 +/- 0.5 pg/15 min (p less than 0 buy minipress .001 vs baseline levels). This cold response to CSF TRH was influenced neither by pretreatment of rats with the alpha-adrenergic blocker phentolamine, administered i.p. (40 mg/kg) or i. c. v. (10(-5) M) 1 h before cold exposure, nor by i. c. v. infusion of the alpha 1-adrenergic blocker prazosin (10(-5) M). In rats receiving the blockers the post-cold TRH peaks were 6.76 +/- 1.61 pg/15 min and 5.70 +/- 0.70 pg/15 min, respectively. The possible origin of CSF TRH and the resistance of its cold stimulation to alpha-adrenergic blockers, compared to TRH released into the median eminence are discussed.

minipress drug interactions 2017-10-07

Systemic administrations (0.1, 0.5, and 2 mg/kg) of alpha1-adrenoreceptor (AR) antagonist prazosin dose-dependently attenuated cold allodynia in a rat tail model of neuropathic pain, whereas alpha2-AR antagonist yohimbine exacerbated it. These results suggest that buy minipress the functions of alpha1- and alpha2-AR in this model are excitatory and inhibitory, respectively, consistent with their general properties. It is also proposed that cold allodynia can be reversed by alpha1-AR antagonist and exacerbated by alpha2-AR antagonist.

minipress dosage forms 2015-08-01

The effects of dopexamine hydrochloride on sympathetic neuroeffector transmission were studied in rabbit isolated pulmonary artery. Short-term exposure of dopexamine (10(-8) x 10(-7) M) and cocaine (10(-6)-3 x 10(-5) M), but not desipramine (3 x 10(-9)-3 x 10(-7) M), to the artery enhanced the contractions evoked by electrical-field stimulation. Corticosterone (4 x 10(-5) M), corticosterone (4 x 10(-5) M) plus cocaine (3 x 10(-8) M), but not cocaine (3 x 10(-5) M), attenuated the enhancement seen with dopexamine. High concentrations of dopexamine (10(-5)-3 x 10(-5) M), cocaine (10(-4) M), and desipramine (10(-6)-10(-5) M) decreased the stimulation-evoked contractions. Dopexamine (10(-7)-3 x 10(-5) M), but neither cocaine nor desipramine, caused an increase in resting tension that waned with time. Corticosterone (4 x 10(-5) M), but not cocaine (3 x 10(-5) M), attenuated the increase in resting tension. Propranolol (10(-6) M) did not alter the enhancing and inhibitory effects of dopexamine. A single concentration (10(-7) and 10(-6) M) of either dopexamine or desipramine caused a time-dependent biphasic response as regards the repetitive stimulation-evoked contractions of pulmonary artery: initial enhancement followed by inhibition. The inhibitory effect of dopexamine (10(-6) M) and desipramine (3 x 10(-6) M) seen after prolonged exposure was almost irreversible and partially reversible, respectively, by washing the preparations with drug-free salt solution. Cocaine caused a monophasic steady-state response: either enhancement (10(-5) M) or inhibition (2 x buy minipress 10(-4) M). In both cases, the onset was rapid. The reduction caused by cocaine (2 x 10(-4) M) and by prazosin (10(-9) M) was fully reversed. Dopexamine (10(-5) M) antagonized competitively the contractions evoked by noradrenaline (3 x 10(-9)-10(-4) M). It is concluded that (1) the dopexamine-induced enhancement of neurogenic contractions is not due to either inhibition of neuronal and extraneuronal uptake of noradrenaline or an agonist action on prejunctional beta 2-adrenoceptors; (2) that the dopexamine-induced inhibition of stimulation-evoked contraction is due to an inhibition of postjunctional alpha 1-adrenoceptors; and (3) that the dopexamine-induced increase in resting tension is due to its metabolite methyldopexamine.

minipress nightmares dosage 2016-12-31

Mean (SD) recovery times in hours for the prazosin plus scorpion antivenom group compared with the prazosin alone groups were: sweating 3 (1.1) v 6.6 (2.6); salivation 1.9 (0.9) v 3 (1.9); priapism 4.7 (1.5) v 9.4 (1.5). Mean (SD) doses of prazosin in the groups were 2 (2.3) buy minipress and 4 (3.5), respectively. 32 patients (91.4%, 95% confidence interval 76.9% to 97.8%) in the prazosin plus antivenom group showed complete resolution of the clinical syndrome within 10 hours of administration of treatment compared with eight patients in the prazosin group (22.9%, 11.8% to 39.3%). Patients from the antivenom plus prazosin group recovered earlier (mean 8 hours, 95% CI 6.5 to 9.5) than those in the control group (17.7 hours, 15.4 to 19.9; mean difference -9.7 hours, -6.9 to -12.4). The number of patients whose condition deteriorated to a higher grade was similar in both groups (antivenom plus prazosin four of 35, prazosin alone five of 35). Hypotension was reported in fewer patients in the antivenom plus prazosin group (12 of 35, 34.3%) than in the prazosin group (19 of 35, 54.3%), but the difference was not statistically significant. No difference was noted in change in blood pressure and pulse rate over time between two groups.

minipress 6 mg 2016-03-19

The analgesic effect of dexmedetomidine added to ropivacaine was not reversed by either prazosin or idazoxan. There were no additive or attenuated effects from the pretreatment with ZD 7288 (I(h) current blocker) compared with dexmedetomidine added to ropivacaine. When buy minipress forskolin was administered as a pretreatment to ropivacaine plus dexmedetomidine, there were statistically significant reductions in duration of analgesia at time points 90-180 min (P < 0.0001 for each individual comparison). The duration of blockade for the forskolin (768 μM) followed by ropivacaine plus dexmedetomidine group mirrored the pattern of the ropivacaine alone group, thereby implying a reversal effect.

minipress xl dosage 2016-06-01

It is estimated that 25% to 30% of patients with heart failure (HE) in the United States are black. Compared with nonblack patients, black patients have a reduced ability to produce endogenous nitric oxide, which may be associated with enhanced responsiveness to drugs that increase the delivery of nitric oxide, such as nitrates. When used with nitrates, hydralazine (HYD) acts as an antioxidant and prevents development of buy minipress nitrate tolerance.

minipress xl drug 2016-10-26

Experiments performed buy minipress on random-bred rat pups showed that muscle training during earlier terms of postnatal ontogeny produce more pronounced changes in the pumping function of the heart.

minipress drug class 2015-03-11

Primary care in buy minipress the UK.

minipress generic name 2017-04-15

The authors investigated whether war-related posttraumatic stress disorder (WR-PTSD) is associated with a postmortem change in neuronal counts in the locus coeruleus (LC) since enhanced central nervous system (CNS) noradrenergic postsynaptic responsiveness has been previously shown to contribute to PTSD pathophysiology. Using postmortem neuromorphometry, the number of neurons in the right LC in seven deceased elderly male veterans was counted. Three veterans were classified as cases of probable or possible WR-PTSD. All three veterans with probable or possible WR-PTSD were found to have substantially lower LC neuronal counts compared to four comparison subjects (three nonpsychiatric veterans and one veteran with alcohol dependence and delirium tremens). To the authors' knowledge, this case series is the first report of LC neuronal counts in patients with PTSD or any other DSM-IV-TR anxiety disorder. Previous postmortem brain tissue studies of Alzheimer's Disease (AD) demonstrated an upregulation of NE biosynthetic capacity in surviving LC neurons. The finding reported is consistent with the similar upregulation of NE biosynthetic capacity of surviving LC neurons in veterans who developed WR-PTSD. Especially if replicated, this finding in WR-PTSD buy minipress may provide further explanation of the dramatic effectiveness of propranolol and prazosin for the secondary prevention and treatment of PTSD, respectively. The LC neurons examined in this study are probably the origin of the first or second "leg" of what might be termed the PTSD candidate circuit. Larger neuromorphometric studies of the LC in veterans with WR-PTSD and in other development-stress-induced and fear-circuitry disorders are warranted, especially using VA registries.

minipress overdose 2017-10-15

Catecholamines and glucocorticoids are involved in fetal maturation of organ systems to prepare the fetus for extrauterine life. Calves, especially when born preterm, depend on function of the adrenergic system and the glucocorticoid axis to adapt energy metabolism for the neonatal period. We tested the hypothesis that hepatic glucocorticoid and α1- and β2-adrenergic receptors in neonatal calves are involved in adaptation of energy metabolism around birth and that respective binding capacities depend on stage of maturation during the neonatal period. Calves (n=7 per group) were delivered by section preterm (PT, 9d before term) or were born at term (full-term, FT; spontaneous vaginal delivery buy minipress ), or spontaneously born and fed colostrum for 4d (FTC). Blood samples were taken immediately after birth and before and 2h after feeding at 24h after birth (PT, FT) or on d 4 of life (FTC) to determine metabolic and endocrine changes. After slaughter at 26h after birth (PT, FT) or on d 4 of life (FTC), liver tissue was obtained to measure hepatic binding capacity of glucocorticoid and α1- and β2-adrenergic receptors. Maximal binding capacity and binding affinity were calculated by saturation binding assays using [(3)H]-prazosin and [(3)H]-CGP-12177 for determination of α1- and β2-adrenergic receptors, respectively, and [(3)H]-dexamethasone for determination of glucocorticoid receptor in liver. Additional liver samples were taken to measure mRNA abundance of glucocorticoid and α1- and β2-adrenergic receptors, of key enzymes and factors related to hepatic lipid metabolism, and of insulin-like growth factor 1 (IGF1). Plasma concentrations of β-hydroxybutyrate and leptin changed with time, and leptin concentrations were affected by stage of maturation. The binding capacities for hepatic glucocorticoid and β2-adrenergic receptors as well as gene expression of IGF1 were greater in FTC than in FT and PT, and binding affinity for β2-adrenergic receptor was lowest in PT. The binding capacity of hepatic α1-adrenergic receptor was greatest in FTC and greater in FT than in PT. The binding capacities of glucocorticoid and α1-adrenergic receptors were mainly related to variables of glucose and lipid metabolism. In conclusion, our results indicate dependence of hepatic glucocorticoid and adrenergic receptors on stage of maturation in neonatal calves and emphasize the association of α1-adrenergic receptor and glucocorticoid receptor with neonatal glucose and lipid metabolism.

minipress 1mg tablet 2016-07-20

Hypertension accelerates the progression of renal disease in patients with chronic renal failure. Doxazosin, an alpha1-antagonist, is an antihypertensive agent with a long half-life. In this study, 15 patients with chronic renal failure were treated only with doxazosin and diuretics for 6 months and their blood pressure, renal parameters and lipid profile were measured. The initial dose of doxazosin was 2 mg/day and it was titrated until blood pressure was normalized. The average dose was 5.6 mg/day. As expected, systolic and diastolic blood pressure were decreased with treatment (165/91 mmHg to 135/73 mmHg). The drop in blood pressure was associated with an increase in glomerular filtration and a decrease in plasma BUN and creatinine levels. Reduction in mean blood pressure and buy minipress decrease in proteinuria had a significant positive correlation (r=0.048, p=0.007). Proteinuria was decreased from 1.8 mg/day to 1.3 mg/day with doxazosin treatment and triglycerides also decreased, while HDL-cholesterol was increased. No side effects were observed. These results indicate that doxazosin is an efficient depressor agent with renal protective actions and that higher doses of doxazosin can be safely given to patients with chronic renal failure.

minipress overdose symptoms 2016-10-07

The pre-gastric rumen of sheep plays a crucial role in the fermentation of nutrients and in the absorption of nutrients and minerals. Adrenaline has been shown previously to increase ruminal absorption of glucose and water. The present study was intended to elucidate whether ruminal ion transport is also altered by adrenaline. In Ussing chambers, changes of I(sc) were recorded in isolated ovine ruminal epithelia after the serosal additions of adrenoceptor agonists or antagonists. I(sc) increased after the addition of adrenaline (10(-4) M) or clonidine (alpha2-agonist, 10(-4) M), but decreased after the addition of isoproterenol (beta-agonist, 10(-4) M) or terbutaline (beta2-agonist, 10(-5) M). The effect of adrenaline on I(sc) was augmented by the adrenoceptor antagonists prazosin (alpha(1), 10(-4) M) and bupranolol (beta, 10(-6) M), but inversed by yohimbine (alpha(2), 10(-5) M). Adrenaline induced an increase in Na+ net flux across the epithelium that was larger than the increase in buy minipress equivalent current flow. It is concluded that adrenaline differentially regulates ion transport across the ruminal epithelium via alpha1-, alpha2-, and beta2-receptors. The main effect is a stimulation of electroneutral and electrogenic Na+ absorption. This stimulated Na+ absorption might be causative of increased water absorption from the rumen as described previously.

minipress overdose death 2016-01-11

Patients with essential hypertension show an increase in vascular resistance. It is unclear whether this is caused by structural changes in the arterial wall or by hyperresponsiveness of vascular smooth muscle to endogenous alpha adrenergic agonists. Using the dorsal hand vein Topamax 5 Mg compliance technique we compared the changes in diameter of superficial veins in response to phenylephrine, an alpha 1 adrenergic receptor agonist, and to nitroglycerin, a venorelaxant, in patients with essential hypertension and in normotensive subjects. The dose of phenylephrine that produced 50% of maximal venoconstriction (ED50) in the hypertensive subjects was 257 ng/min (geometric mean; log mean +/- SD was 2.41 +/- 0.54). In the control subjects the ED50 was 269 ng/min (geometric mean; log mean was 2.43 +/- 0.43). Maximal response (Emax) for phenylephrine was 84 +/- 13% in the hypertensive subjects and 90 +/- 6% in the control subjects. Differences in the group means of the ED50 (P = 0.92) or the Emax (P = 0.27) were not significant. There were no significant differences in the ED50 (P = 0.54) or the Emax (P = 0.08) for nitroglycerin between the two groups. These results show no evidence for a generalized change in alpha adrenergic responsiveness in hypertension and support the concept that increased blood pressure responses to alpha adrenergic stimulation in hypertensives are due to structural and geometric changes in the arterial wall rather than to an increased responsiveness of postsynaptic alpha adrenergic receptors. The phenylephrine studies were repeated in seven hypertensive patients during treatment with prazosin, an alpha 1 adrenergic antagonist. The mean dose ratio of the shift in phenylephrine ED50 (ED50 during prazosin therapy/ED50 before prazosin therapy) was 6.1. This indicates that small doses of prazosin (1-2 mg) cause significant in vivo shifts in the dose-response relationship of alpha adrenergic agonists. The dorsal hand vein compliance technique is useful in detecting systemic effects of alpha adrenergic antagonists.

minipress xl tablets 2017-03-25

Prostatic A2A adenosine receptors mediate varied effects. This study aimed to test whether genetic disruption of this receptor affects prostate contractility. Prostates taken from mice which were homozygous (A2AR-/-) and heterozygous (A2AR+/-) for the disrupted A2A adenosine receptor gene and wild-type littermates (A2AR +/+) were mounted in organ baths. Contractile responses to nerve stimulation and noradrenaline were measured in the presence of various pharmacological tools. Electrical field stimulation (0.5 ms pulse duration, 60 V, 0.1-20 Hz) yielded frequency-dependent contractions while exogenous administration of noradrenaline (10 nM-1 mM) or tyramine (1 microM-1 mM) produced concentration-dependent responses. Contractile responses to electrical field stimulation from A2AR-/- and A2AR+/- prostates were reduced when compared to A2A+/+ prostates (P=0.013, n=33-36). Prazosin (0.3 microM) inhibited electrical field stimulation-induced responses in prostates from A2AR+/+ and A2AR+/- mice (P< or =0.016, n=5-7) but not A2AR-/- mice (P=0.400, n=6). Tetrodotoxin abolished electrical field stimulation-induced responses in all prostates (P<0.001, n=5 Anafranil 10mg Dosage -7). NF 449 and ZM 241385 were without effect (P< or =0.421, n=4-6). There were no genotype differences in noradrenaline or tyramine concentration-response curves (P> or =0.180, n=10-13). Prazosin (0.3 microM) and cocaine (10 microM) attenuated the responses induced by noradrenaline (P<0.001, n=6-7) and tyramine (P<0.001, n=5-6), respectively, in all genotypes. Disruption of the A2A adenosine receptor leads to reduced nerve mediated contractile responses of the prostate in mature mice.

minipress capsules 2016-04-16

Recent evidences from molecular biology, radioreceptor binding and functional studies indicate that the alpha 1-adrenoceptor population is heterogeneous and can at least be divided into two subclasses named alpha 1A and alpha 1B. The present study was designed to obtain, a selective enrichment of rat brain cortical membranes with each subtype of alpha 1-adrenoceptor using alkylating agents. [3H]prazosin binding to rat cortical membranes was saturable and of high affinity (KD = 0.11 +/- 0 Diflucan User Reviews .02 nM; Bmax = 132.5 +/- 7.2 fmol/mg protein). All ligands competed for specific [3H]prazosin binding in a statistically significant biphasic manner (%Rhigh = 30-40%; %Rlow = 60-70%). These sites meet generally accepted and recently described pharmacologic criteria for their identification as the alpha 1A- and alpha 1B-adrenoceptors. After pretreatment of membranes with benextramine (1 microM) in the presence of clonidine (1 microM), the antagonists, WB4101, (+)-niguldipine and phentolamine, displaced the radioligand with an inhibition curve steeper than in control membranes and with Ki values that agree with those obtained for the low affinity site present in control membranes. On the other hand, after pretreatment with chloroethylclonidine (10 microM) in the presence of WB4101 (1 nM), Hill coefficients for the displacement of the radioligand by WB4101, (+)-niguldipine, and phentolamine, were also increased, but in contrast to the situation described above, the Ki values agree with those obtained for the high affinity site present in control membranes. In conclusion, this method of partial alkylation of receptors could be a valuable tool for separately studying the pharmacological characteristics of the alpha 1-adrenoceptor subtypes in native membranes of cerebral tissue.

minipress medication information 2015-10-08

Since the end of the 1980s, the pathological importance of baroreflex function has attracted the attention of many investigators. In our Detrol Generic previous studies, it was found that ketanserin lowered blood pressure (BP), decreased BP variability and enhanced baroreflex sensitivity (BRS). The present work was designed to test the hypothesis that the restoration of BRS by ketanserin is not dependent on BP level in conscious rats.

minipress and alcohol 2016-04-11

We randomised ambulatory men with diastolic blood pressure (BP) 95-109 mmHg without anti-hypertensive medication to single drug treatment with either hydrochlorothiazide 12.5-50 mg/day, atenolol 25-100 mg/day, captopril 25-100 mg/day, clonidine 0.2-0.6 mg/day, diltiazem-SR 120-360 mg/day, prazosin 4-20 mg/day or placebo in a double-blind prospective trial. The assigned drug was titrated to a goal BP of < 90 mm Hg. Patients not achieving goal BP were rerandomised to an alternative single active drug. Non-responders to the second drug received the first drug in combination with the second. Of Urispas Dosage Adults the 102 non-responders to both drugs who qualified for the combination, 59 (57.8%) responded. The combination pairs that included a diuretic achieved diastolic goal BP in 69% and < 140 mm Hg systolic in 77% compared with 51% and 46%, respectively, for those combinations without a diuretic (P = 0.067; P = 0.002). Six of the eight terminations due to adverse drug reactions were in combinations containing prazosin; three of these six were hypotensive reactions. We conclude that two single drugs of insufficient efficacy to control BP individually have a high probability of achieving goal BP when combined, especially if the combination contains a diuretic.

minipress user reviews 2016-09-15

The effect of four calcium antagonists (nifedipine, nitrendipine, nisoldipine, and verapamil) on hypoxia-induced changes in right ventricular parameters were examined in anesthetized closed-chest rats using an ultraminiature catheterization technique. The effect of the calcium antagonists was compared to the alpha-adrenoceptor blocker prazosin, the beta-adrenoceptor blocker propranolol, the angiotensin-converting enzyme (ACE) inhibitor captopril, and the vasodilator nitroglycerin. The animals were exposed to two successive 5-min hypoxic periods separated by a normoxic interval of 60 min, during which the animals received an intravenous (i.v.) infusion of the substances tested. Hypoxia caused a marked rise in right ventricular systolic pressure (RVSP) and a moderate increase in RVdP/dtmax. Heart rate (HR) was only slightly enhanced. The functional response to the second hypoxic period did not differ from the first one in NaCl-infused animals. All calcium antagonists reduced the hypoxic pressure increase in a dose-dependent manner and ultimately abolished it. Nisoldipine was the most effective substance, followed by nifedipine, nitrendipine, and verapamil. In contrast, prazosin and propranolol did not influence the hypoxic pressure response. Administration of captopril and nitroglycerin attenuated the increase in RVSP. Thus, as compared with the other substances tested, calcium antagonists were the most effective drugs that antagonized the hypoxia-induced increase in Parlodel 5 Mg RVSP.

minipress tablets dose 2017-01-11

A tertiary care hospital in south Glucophage Y Alcohol India.

minipress reviews 2017-11-11

To determine the efficacy Ceftin Medicine of terazosin as a facilitator agent for the passage of lower ureteral stones.

minipress 1mg capsule 2017-12-23

We have investigated the ability of alpha(1 Antabuse Tablets Images )-adrenoceptor antagonists to affect the hyperthermia produced by methylenedioxy methamphetamine (MDMA) in conscious mice.

minipress 2 mg 2015-11-08

In this study the effects of a single daily dose (average 8.9 mg) of doxazosin (an alpha-adrenergic blocker) given at night were evaluated in 111 patients with mild hypertension. Patients were studied first on no medication, and a second time after being treated for up to 16 weeks with doxazosin. Blood pressure was measured by noninvasive ambulatory monitoring at the beginning and end of the study. There was a sustained reduction of both systolic and diastolic pressure throughout the day and night, but the greatest reduction occurred in the morning hours. Since the peak treatment effect was later than predicted from previous pharmacokinetic studies, it is suggested that the timing of the peak effect may depend on the prevailing level of alpha-adrenergic tone, as well as on the pharmacokinetics of the drug Singulair Medication .

tab minipress dosage 2016-07-22

The effects of intracerebroventricular (icv) administration of somatostatin(1-14) (SS1-14) on mean arterial blood pressure (MAP), heart rate (HR), plasma arginine vasopressin (AVP) concentration, and splanchnic nerve activity (SpNA) were studied in conscious rats. In addition, the effects of peripheral alpha-adrenergic receptor blockade with prazosin, vasopressinergic V1-receptor blockade with [d(CH2)5Tyr(Me)]AVP, and chronic bilateral sinoaortic denervation (SAD) on central SS1-14-induced MAP, HR, and SpNA responses were investigated. SS1-14 icv elicited dose-dependent increases in MAP and plasma AVP concentration as well as decreases in HR and SpNA. Prazosin iv did not significantly affect SS1-14-induced pressor and bradycardic responses but augmented the decrease in SpNA. The V1-AVP receptor antagonist iv significantly attenuated the effects of SS1-14 icv on MAP, HR, and SpNA. Following SAD the pressor responses to Imitrex Pill Identifier SS1-14 icv were significantly enhanced and were associated with significantly smaller decreases in HR and SpNA. We conclude that central administration of SS1-14 causes a pressor response via release of AVP while at the same time inhibiting peripheral sympathetic outflow. Our results support the hypothesis that SS1-14 in the brain by its effects on AVP release and sympathetic outflow may participate in central cardiovascular regulation.

minipress medicine 2017-06-15

The antihypertensive effect and safety of doxazosin once daily as well as the effect on serum lipids was compared with that of atenolol once daily in 40 patients with mild to moderate hypertension. During the first 4 weeks, all patients received placebo therapy. During the subsequent 46 weeks, patients were randomized to doxazosin or atenolol treatment. Treatment was initiated with 1 mg doxazosin or 50 mg atenolol once daily. The dose could be doubled biweekly for 10 weeks until a final dose of 16 mg doxazosin or 100 mg atenolol was reached. The patients then entered the maintenance phase for 36 weeks. The average final dose of doxazosin was 9.2 +/- 1.3 (SEM) mg and that of atenolol was 76.5 +/- 6.2 mg. During the 46 weeks of active treatment, the recumbent diastolic blood pressure (DBP) tended to be lower (p less than 0.05) in patients receiving atenolol at 10, 12, and 22 weeks of treatment. Recumbent systolic BP (SBP) and standing SBP and DBP were not different, however, between patients receiving doxazosin and those receiving atenolol. Recumbent and standing heart rate (HR) were lower (p less than 0.01) during atenolol. The decrease in serum total triglycerides, total cholesterol, and low-density lipoprotein (LDL)-cholesterol after 46 weeks of doxazosin was different (p less than 0.05) from the changes observed during atenolol therapy. Our data indicate that the antihypertensive action of doxazosin is accompanied by favorable effects on serum lipids.

minipress drug information 2015-08-08

The effects of ATP and related purine compounds, NG-nitro-L-arginine (NOARG; an inhibitor of nitric oxide synthesis from L-arginine), calcitonin gene-related peptide (CGRP), substance P and vasoactive intestinal polypeptide (VIP) on relaxation and smooth muscle tension induced by electrical field stimulation (EFS) were studied in isolated male rabbit circular urethral smooth muscle (functional study). In addition, the outflow of ATP elicited by EFS was measured using the luciferase technique (superfusion study). All experiments were performed in the presence of guanethidine (3 x 10(-3) mol/L) and atropine (10(-6) mol/L).