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Morbihan's disease (MD), also known as 'persistent facial oedema' or 'rosaceous lymphoedema', is an uncommon facial condition that is difficult to treat. Its cause remains unclear.
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MI was induced by ligation of the coronary artery in Wistar rats, which were separated into (1) vehicle-treated group, (2) CAN-treated group (10 mg/kg per day), (3) SPIRO-treated group (100 mg/kg per day) and (4) CAN + SPIRO-treated group. The activity of both AP-1 and NF-kappaB was significantly increased at 4 weeks after MI. CAN or SPIRO significantly prevented the cardiac remodeling and activity of AP-1 and NF-kappaB. Furthermore, CAN + SPIRO prevented the cardiac remodeling and activation of AP-1 and NF-kappaB, compared with CAN or SPIRO alone. Myocardial atrial natriuretic peptide, brain natriuretic peptide, collagen I and III mRNAs were enhanced by MI, and CAN or SPIRO alone significantly reduced the mRNAs. CAN + SPIRO significantly prevented these mRNAs, compared with CAN or SPIRO alone.
Currently there are 4 to 5 million people with congestive heart failure in the United States. They consume greater than 7% of the total health care dollar of which a significant portion is directly related to hospitalization expenses alone. Most patients with chronic congestive heart failure can be managed efficiently outside the hospital setting by the proper use of nonpharmacologic therapies. Neurohormonal pathways have a significant impact on the progression of congestive heart failure. Medications, which include alpha-blockers, beta-blockers, digoxin, spironolactone, and diuretics, now can block, modify, or manage most of these neurohormonal effects, and therefore, have a stabilizing effect on the patient with congestive heart failure. Understanding the physiology and medications involved for optimal treatment of congestive heart failure is a must to ensure the quality of life that these patients deserve.
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Resistant hypertension has for many decades been defined as difficult-to-treat hypertension in order to identify patients who may benefit from special diagnostic and/or therapeutic considerations. Recently, the term "refractory hypertension" has been proposed as a novel phenotype of antihypertensive failure, that is, patients whose blood pressure cannot be controlled with maximal treatment. Early studies of this phenotype indicate that it is uncommon, affecting less than 5% of patients with resistant hypertension. Risk factors for refractory hypertension include obesity, diabetes, chronic kidney disease, and especially, being of African origin. Patients with refractory are at high cardiovascular risk based on increased rates of known heart disease, prior stroke, and prior episodes of congestive heart failure. Mechanisms of refractory hypertension need exploration, but early studies suggest a possible role of heightened sympathetic tone as evidenced by increased office and ambulatory heart rates and higher urinary excretion of norepinephrine compared to patients with controlled resistant hypertension. Important negative findings argue against refractory hypertension being fluid dependent as is typical of resistant hypertension, including aldosterone levels, dietary sodium intake, and brain natriuretic peptide levels being similar or even less than patients with resistant hypertension and the failure to control blood pressure with use of intensive diuretic therapy, including both a long-acting thiazide diuretic and a mineralocorticoid receptor antagonist. Further studies, especially longitudinal assessments, are needed to better characterize this extreme phenotype in terms of risk factors and outcomes and hopefully to identify effective treatment strategies.
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Recent evidence suggests that treatment with mineralocorticoid receptor antagonist suppressed local inflammation in vascular tissues or cardiomyocytes; therefore, we examined the effect of spironolactone on glucose and lipid metabolism in a mouse model with diet-induced diabetes and nonalcoholic fatty liver disease. C57BL/6 mice were fed either the control diet, 60% fat diet with 30% fructose water (HFFD), or HFFD with spironolactone for 8 wk. HFFD mice demonstrated apparent phenotypes of metabolic syndrome, including insulin resistance, hypertension, dyslipidemia, and fatty liver. Although treatment with spironolactone did not affect the increased calorie intake and body weight by HFFD, the increments of epididymal fat weight, blood pressure, serum triglyceride, free fatty acids, leptin, and total cholesterol levels were significantly suppressed. Elevation of blood glucose during glucose and insulin tolerance tests in HFFD mice was significantly lowered by spironolactone. Notably, increased glucose levels during pyruvate tolerance test in HFFD mice were almost completely ameliorated to control levels by the treatment. Staining with hematoxylin-eosin (HE) and Oil-red-O demonstrated marked accumulation of triglycerides in the centrilobular part of the hepatic lobule in HFFD mice, and these accumulations were effectively improved by spironolactone. Concomitantly HFFD feeding markedly up-regulated hepatic mRNA expression of proinflammatory cytokines (TNFalpha, IL-6, and monocyte chemoattractant protein-1), gluconeogenic gene phosphoenolpyruvate carboxykinase, transcription factor carbohydrate response element binding protein, and its downstream lipogenic enzymes, all of which were significantly suppressed by spironolactone. These results indicate that inhibition of mineralocorticoid receptor might be a beneficial therapeutic approach for diet-induced phenotypes of metabolic syndrome and fatty liver.
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Traditionally, the role of aldosterone in heart failure was thought to be a result of its effects on epithelial cells where it induces sodium reabsorption and potassium excretion with subsequent haemodynamic effects from intravascular volume expansion. On this basis, spironolactone, a non-selective aldosterone antagonist, has been used for the treatment of congestive heart failure to block aldosterone-mediated effects in epithelial cells. The Randomized Aldactone Evaluation Study (RALES), in which spironolactone was added to existing therapy in patients with heart failure, showed a significant reduction in morbidity and mortality. These results suggest that the role of aldosterone in the pathophysiology of cardiovascular disease may be more complex than previously recognised. There now is extensive experimental and growing clinical evidence for an important physiological role for aldosterone in the pathology of cardiac and renal disease. Classical effects of aldosterone are mediated via its nuclear receptor. Novel non-epithelial effects of aldosterone are mediated via a second messenger system, which involves activation of the sodium/hydrogen antiporter. These effects of aldosterone have been demonstrated in the kidney, vascular smooth muscle cell and leukocytes, and in the regulation of rapid corticotropin suppression. It has been hypothesised that cardiac damage induced by aldosterone is independent of the presence of hypertension. In support of this, experimental evidence demonstrates that cardiovascular damage induced by aldosterone can be prevented by administration of a selective mineralocorticoid receptor antagonist. These findings suggest the dissociation between cardiovascular lesions and high blood pressure, and highlight the importance of aldosterone in the pathological changes.
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Of the 2292 prescriptions with at least one antihypertensive prescription frequencies are: ARB (43%), diuretics (43%), beta-blockers (34%), CCB (26%), ACEI (26%), spironolactone (8%), central and alpha (7%), DRI (1%). The prescription is performed as monotherapy (42%), bitherapy (37%), triple therapy (16%) and quadruple or more (5%). When triple therapy is prescribed, there is an association ACEI or ARB or DRI+Diu+BB in 46%, and an association ACEI or ARB or DRI+Diu+AC in 30%. Cardiovascular disease is present or past reported by 24% of hypertensive patients: coronary artery disease (13%), heart failure (6%), arrhythmias (5%), stroke (4%), PAD (4%). The use of BB is more common in hypertensive patients who have coronary artery disease, heart failure and arrhythmia. ACE inhibitors are more common in hypertensive patients with coronary artery disease, heart failure or stroke. CCB are more frequent in cases of coronary artery disease or PAD. The ARB are less frequent in patients with coronary artery disease.
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Estimated glomerular filtration rate (eGFR) showed an acute fall in the first month of treatment (5.1 ± 9.4 mL/min/1.73 m(2)), but it remained stable thereafter (+0.04 ± 0.7 mL/min/1.73 m(2)/month), with a significant difference with respect to the eGFR slope during the 12-month pre-treatment period. The initial eGFR fall predicted a more stable course of renal function, the higher the eGFR initial fall, the better the long-term evolution of eGFR. Proteinuria showed an important and sustained reduction since the first month of treatment. At the end of follow-up, it had decreased by 61% (43-77%) with respect to baseline values. The antiproteinuric and renoprotective influence of spironolactone was also observed in diabetic patients and in patients with renal function impairment, although tolerance was poorer among the latter.
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This study employed an in vitro system to identify potential steroidal mediators of spermiation in Bufo arenarum. Testicular fragments were incubated for 2 h at 28 degrees. Spermiation was induced by 10 IU human chorionic gonadotropin (hCG) and the effect of different inhibitors of steroid biosynthesis was analyzed. Cyanoketone (10(-5)-10(-6) M), an inhibitor of 3-oxo-4-ene steroid biosynthesis, did not block hCG-inducing activity even when biosynthesis of 3-oxo-4-ene steroids and its reduced metabolites was inhibited by 95%. Aminogluthetimide at a concentration that inhibited testosterone biosynthesis (10(-4) and 10(-5) M) did not alter hCG actions. Similar results were obtained with spironolactone, an inhibitor of 17alpha-hydroxylase/17-20 lyase activity. No spermiation-inducing activity was found with different steroids (progesterone, 17-hydroxypregnenolone, 17, 20alpha/beta-dihydroxy-4-pregnene-3-one, estradiol, testosterone, etc.). It is concluded that spermiation induced by hCG is not steroid mediated in B. arenarum.
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When administered after MI, eplerenone prevents cardiac remodelling accompanied by systolic and diastolic dysfunction and inhibits abnormal myocardial transcriptional activities and gene expression.
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Cardiovascular diseases, such as arterial hypertension, heart failure, coronary artery disease, peripheral circulatory problems and atrial fibrillation are increasingly present in aged patients. Comorbidities, mainly diabetes, renal dysfunction, chronic bronchitis and degenerative joint diseases, are also frequent and need additional drug treatment. The usual polypharmacy often causes side effects due to overdosage and/or drug interactions. The main difficulty in choosing the proper therapeutic regimen consists in the lack of suitable dosing guidelines with adapted therapeutic targets for the older multimorbid population, usually not represented in the large controlled trials forming the basis of general recommendations. European guidelines for hypertension and heart failure are discussed as examples.
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Aldosterone promotes nephrosclerosis in several rat models, whereas aldosterone receptor antagonism blunts the effect of activation of the renin-angiotensin-aldosterone system (RAAS) on nephrosclerosis, independent of effects on blood pressure. Based on recent findings linking activation of the RAAS with impaired fibrinolytic balance, we hypothesized that aldosterone induces sclerosis through effects on plasminogen activator inhibitor-1 (PAI-1), the major physiological inhibitor of plasminogen activation.
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Forty-two patients with confirmed primary aldosteronism (21 with aldosterone-producing adenoma treated by unilateral laparoscopic adrenalectomy, 21 treated with spironolactone) were investigated by carotid ultrasound at baseline and 1 and 6 years after the specific treatment.
Socioeconomic deprivation is associated with increased heart failure (HF) incidence, hospitalization rates, and mortality. However, whether the delivery of survival-enhancing medical therapy is equitable remains uncertain. We examined secular trends in the uptake of key medical therapies (angiotensin-converting enzyme inhibitors or angiotensin receptor blockers, β-blockers, spironolactone) stratified by socioeconomic circumstances in patients with HF. Secondary analyses examined trends in HF incidence, prevalence, and survival.
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During study follow-up, more UC patients had an unplanned readmission for any cause (44% vs. 22%: P=0.019, OR 1.95 95% CI 1.10-3.48) whilst 7 (15%) versus 5 (9%) UC and C+HBI patients, respectively, died (P=NS). Overall, 15 (26%) C+HBI versus 21 (44%) UC patients experienced a primary endpoint. C+HBI was associated with a non-significant, 45% reduction in the risk of death or readmission when adjusting for potential confounders (RR 0.55, 95% CI 0.28-1.08: P=0.08). Overall, C+HBI patients accumulated significantly fewer unplanned readmissions (15 vs. 45: P<0.01) and days of recurrent hospital stay (108 vs. 459 days: P<0.01). C+HBI was also associated with greater uptake of beta-blocker therapy (56% vs. 18%: P<0.001) and adherence to Na restrictions (P<0.05) during 6-month follow-up.
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Primary aldosteronism occurs in 1-10% of hypertensive patients and is classified in adenomas or bilateral adrenal hyperplasia. Computed tomography (CT) or magnetic resonance imaging can be used to discriminate these subtypes and in guiding treatment selection. This case report describes a 65-year-old man with hypertension and hypokalaemia during 25 years. Bilateral adrenal hyperplasia was diagnosed based on a CT, and an oral sodium-loading test with measurement of renin and aldosterone confirmed the diagnosis. Blood pressure and potassium in plasma was normalized during treatment with the mineralocorticoid receptor antagonist eplerenon.
Ten subjects (median age 28 years) were enrolled and completed the protocol. The median flow-mediated dilation at baseline was 9.1% and did not change significantly after 4 weeks of spironolactone 7.6%, P = .46. There was mild elevation in serum cytokine profiles and only interleukin-1b decreased significantly with therapy, 0.39 to 0.23 pg/mL, P = .04.
We previously reported that aldosterone impaired vascular insulin signaling in vivo and in vitro. Fructose-enriched diet induces metabolic syndrome including hypertension, insulin resistance, hyperlipidemia and diabetes in animal. In the current study, we hypothesized that aldosterone aggravated fructose feeding-induced glucose intolerance in vivo. Rats were divided into five groups for six-week treatment; uninephrectomy (Unx, n=8), Unx+aldosterone (aldo, 0.75 µg/h, s.c., n=8), Unx+fructose (fruc, 10% in drinking water, n=8), Unx+aldo+fruc, (aldo+fruc, n=8), and Unx+aldo+fruc+spironolactone, a mineralocorticoid receptor antagonist (aldo+fruc+spiro, 20mg/kg/day, p.o., n=8). Aldo+fruc rats manifested the hypertension, and induced glucose intolerance compared to fruc intake rats assessed by oral glucose tolerance test, homeostasis model assessment of insulin resistance and hyperinsulinemic-euglycemic clamp study. Spironolactone, significantly improved the aldosterone-accelerated glucose intolerance. Along with improvement in insulin resistance, spironolactone suppressed upregulated mineralocorticoid receptor (MR) target gene, serum and glucocorticoid-regulated kinases-1 mRNA expression in skeletal muscle in aldo+fruc rats. In conclusion, these data suggested that aldosterone aggravates fructose feeding-induced glucose intolerance through MR activation.
To evaluate the influence of spironolactone on serum potassium in decompensated heart failure (HF).
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In patients with hypertension and chronic renal parenchymal disease, BP should be controlled to 130/85 mmHg or lower (125/75 mmHg) in patients with proteinuria in excess of 1 g/day. Reducing dietary sodium (< 7 g/day) and protein (< 0.6-0.7 g/kg) helps control high BP and renal function in patients with renal insufficiency. As first antihypertensive drug, ACE inhibitors or long-acting Ca antagonists are recommended. In patients with renovascular hypertension, angioplasty is the first choice increasingly to be accompanied by stenting, and surgical revascularization is the next choice. As antihypertensive drugs, beta blockers, ACE inhibitors, and AII-receptor blockers are recommended. Hypertension accompanied by endocrine disease with adenoma or tumor is almost cured or improved by surgical removal. Spironolactone and Ca antagonists are used in patients with idiopathic aldosteronism (bilateral hyperplasia). Alpha and beta blockers are used in patients with pheochromocytoma during preoperative period.
A total of 32 167 UTC patients with hypertension were enrolled in the National Health Insurance program between 2005 and 2011.
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There are several ion-transport systems expressed in the lower intestinal segments of chickens, depending on the level of the salt intake. The aim of this study was to test the hypothesis that aldosterone is the sole regulator of all these ion-transport systems, as had been indicated by our previous results. Chickens were long-term adapted to low salt intake, and then switched to a high-salt diet. During the first 5 days of resalination, the birds were injected with aldosterone every 8 hr and then the magnitude and characteristics of the epithelial ion-transport systems in colon and coprodeum were investigated. The results support strongly the hypothesis that aldosterone exerts major control of the amiloride-inhibitable Na(+)-transport system in both colon and coprodeum, as its magnitude was maintained high in spite of the resalination process. Spironolactone counteracted the actions of aldosterone, although not totally. On the other hand, aldosterone is not the sole regulator of the hexose/aminoacid-Na+ cotransport systems in colon, although it can act as their modulator, as the injections did delay the normal increase always seen in these transport systems during resalination. Aldosterone can also modulate the Cl(-)-secretory capacity of colon and coprodeum, but only temporarily.
A sixty-one year old Caucasian female with long-standing poorly-controlled hypertension was referred with multiple drug intolerances. She was unable to take Amlodipine, Nifedipine, Lercanidipine, Lisinopril, Candesartan, Bendroflumethiazide, Indapamide, Spironolactone, Amiloride, Doxazosin, Bisoprolol due to unacceptable side effects. After multiple pharmacotherapeutic attempts over a one year period, she could only tolerate Nebivolol 2.5 mg daily, liquid Nifedipine solution 16 mg twice daily and one quarter Glyceryl trinitrate (GTN) 5 mg transdermal patch daily. Despite this BP control remained suboptimal and she was offered treatment with the ROX coupler device having declined renal denervation for personal reasons.
Although the presence of mineralocorticoid binding sites have been demonstrated in brain, little is known about their physiological role. The purpose of this study was to evaluate possible interactions between a relatively short 2-day central infusion of aldosterone (5 ng/h) and a diverse group of centrally acting pressor agents. The intracerebroventricular infusion of aldosterone selectively attenuated the pressor response produced by the injection of arginine vasopressin (AVP, 10-400 ng) into the lateral ventricle without altering the responses to ventricular administration of 50-200 ng angiotensin II (ANG II), 150 ng carbachol, and 0.5 and 1 M hypertonic sodium chloride. No aldosterone-vasopressin interaction occurred in rats receiving a simultaneous central infusion of aldosterone and RU 28318 [7 beta-hydroxy-3-oxo-7 alpha-propyl(17 alpha)-pregn-4-ene-21-potassium carboxylate], a specific mineralocorticoid receptor antagonist. Baroreflex reactivity and the pressor response to intravenous AVP were not modified by the aldosterone treatment, indicating that overall cardiovascular reactivity was not depressed. Because the vascular reactivity of the mesenteric artery to AVP and norepinephrine remained unchanged after 2 days of central aldosterone infusion, and because plasma levels of aldosterone were not altered, the selective inhibition by this mineralocorticoid of the central AVP response appears to be purely central in origin. This specific central effect of aldosterone is mediated through interaction with mineralocorticoid receptors.
Altering the renin-angiotensin aldosterone system improve mortality in heart failure (HF) in part through an improvement in nitric oxide (NO)-mediated endothelial function. This study examined if spironolactone affects endothelial nitric oxide synthase (eNOS) and NO-mediated vasorelaxation in HF.
A method of assessing the qualitative and quantitative activity of competitive aldosterone antagonists in healthy man is described. It requires intravenous infusion of aldosterone (0.5 mg/6 h), iv and oral water loading for six hours and fractionated collection of urine over eight hours. Aldosterone antagonists were administered orally 1.5 h before the start of the infusion (spironolactone 50, 200 or 800 mg) or added to the infused solution (potassium cnarenoate 300, 600 or 1000-1200 mg). The effect was assessed by changes in urinary sodium and potassium excretion and in urinary Na+/K+ ratio. The plasma levels and urinary excretion of canrenone, canrenoate and canrenoate ester glucuronide, respectively, were determined after administration of spironolactone and potassium canrenoate. Between 4-8 h (spironolactone) or 2-8 h (potassium canrenoate) after commencement of the infusion there was linear dose-dependent reversal of the mineralocorticoid-induced sodium retention and/or decrease in the Na+/K+ ratio. The plasma levels and urinary excretion of the metabolites measured were also dose-dependent. The method appears suitable for comparison of the potency of aldosterone antagonists and for defining the time course of drug action within the observation period employed.
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Spironolactone lowers portal hypertension by improvement of liver fibrosis and inhibition of intrahepatic vasoconstriction via down-regulating ROCK-2 activity and activating NO/PKG pathway. Thus, early spironolactone therapy might be the optional therapy in cirrhosis and portal hypertension.
Cortisol levels did not differ between lean and obese after placebo. Spironolactone and RU38486 alone had modest effects, increasing cortisol by less than 50% in both groups. However, combined spironolactone plus RU38486 elevated cortisol concentrations substantially, more so in lean than obese men [2.9- (0.3) vs. 2.2 (0.3)-fold elevation, P = 0.002].
Activation of the renin-angiotensin-aldosterone system is associated with unsatisfactory outcomes in patients with hypertension and heart failure in that activation of this system is correlated strongly with both the incidence and extent of end-organ damage. Despite the availability of the angiotensin converting enzyme inhibitors (ACEi) and the angiotensin receptor blockers (ARB), unblocked aldosterone levels remain an important risk factor for cardiovascular disease progression. New preclinical data generated over the last few years strongly supports the hypothesis that aldosterone has important deleterious effects on the cardiovascular system independent of the classical action of this hormone on renal epithelial cells. The new selective aldosterone blocker, eplerenone, has been shown to produce significant cardioprotective and renoprotecive effects in experimental models of cardiovascular disease. Early clinical studies suggests that eplerenone may have important therapeutic benefit in the treatment of hypertension and heart failure post-myocardial infarction (post-MI).