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Diovan (Valsartan)

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Diovan is a high-quality medication which is taken in treatment of hypertension. It is used in the treatment of heart failure and to reduce the risk of death after a heart attack. It is working by preventing the hormone angiotensin II from narrowing the blood vessels, which tends to raise blood pressure.

Other names for this medication:

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Lasix, Norvasc, Toprol, Hyzaar, Teveten, Benicar, Edarbi, Micardis, Cozaar, Atacand, Avapro


Also known as:  Valsartan.


Diovan is an effective remedy against hypertension. Its target is to treat heart failure and to reduce the risk of death after a heart attack.

It is working by preventing the hormone angiotensin II from narrowing the blood vessels, which tends to raise blood pressure. It is angiotensin II receptor antagonist.

Diovan is also known as Valsartan, Valtan, Valzaar.

Generic name of Diovan is Valsartan.

Brand name of Diovan is Diovan.


To treat high blood pressure: 80 mg or 160 mg or more once a day. The maximum dosage is 320 mg a day.

To treat heart failure: 40 mg twice a day.

The maximum dosage is 320 mg daily.

Take Diovan tablets orally with or without food.

Do not crush or chew it.

Take Diovan at the same time every day with water.

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


If you overdose Diovan and you don't feel good you should visit your doctor or health care provider immediately. Symptoms of Diovan overdosage: fainting, abnormal heartbeats, lightheadedness.


Store at room temperature between 15 and 30 degrees C (59 and 86 degrees F) away from moisture and heat. Keep your medicine container tightly closed. Throw away any unused medicine after the expiration date. Keep out of the reach of children.

Side effects

The most common side effects associated with Diovan 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 Diovan if you are allergic to Diovan components.

Do not take Diovan if you're pregnant or you plan to have a baby, or you are a nursing mother. Diovan can harm your baby.

Take Diovan with care if you are taking any other blood pressure medications: diuretic (water pill) such as amiloride (Midamor), spironolactone (Aldactone), triamterene (Dyrenium, Maxzide, Dyazide), angiotensin-converting enzyme (ACE) inhibitors such as benazepril (Lotensin), captopril (Capoten), enalapril (Vasotec), fosinopril (Monopril), lisinopril (Prinivil, Zestril), moexipril (Univasc), perindopril (Aceon), quinapril (Accupril), and trandolapril (Mavik); beta blockers such as atenolol (Tenormin), labetalol (Normodyne), metoprolol (Lopressor, Toprol XL), nadolol (Corgard), propranolol (Inderal), ramipril (Altace).

Be careful with Diovan if you suffer from or have a history of liver disease, kidney disease.

Do not use potassium supplements or salt substitutes.

If you want to achieve most effective results without any side effects it is better to avoid alcohol.

Do not stop taking Diovan suddenly.

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In patients with HF and reduced EF enrolled in PARADIGM-HF, LVEF was a significant and independent predictor of all outcomes. Sacubitril/valsartan was effective at reducing cardiovascular death and HF hospitalization throughout the LVEF spectrum.

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The available angiotensin II type 1 (AT(1))-receptor blockers differ markedly in their pharmacological properties and clinical efficacy. Losartan shifts the dose-response curve for angiotensin II to the right without affecting the maximal response; this antagonism can be overcome by increasing concentrations of angiotensin II and thus losartan acts as a surmountable antagonist. By contrast, other agents suppress the maximal response to angiotensin II to varying extents; this can not be overcome by increasing angiotensin concentrations and hence these agents are insurmountable antagonists. Receptor binding studies have shown that candesartan has the highest affinity for the AT(1)-receptor, followed by irbesartan, valsartan and losartan, and that candesartan dissociates from the receptor more slowly than other antagonists. A meta-analysis using an E(Max) model has shown that differences in receptor binding activity are reflected in differences in maximal antihypertensive effect, and this finding is supported by the results of comparative clinical trials. Moreover, the prolonged binding of candesartan to the receptor is reflected in a longer duration of action, compared with losartan; the antihypertensive effect of candesartan persists for 48 h after dosing, compared with approximately 24 h with losartan. Candesartan thus offers extended therapeutic coverage, an important consideration since a majority of patients miss occasional doses of antihypertensive medication. There is currently no evidence that differences in receptor binding between AT(1)-receptor blockers translate into differences in tolerability. In summary, therefore, pharmacological differences between AT(1)-receptor blockers are reflected in clinically important differences in maximal antihypertensive effect, response rate, and duration of action.

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Increased arterial stiffness, as estimated from aortic pulse wave velocity (Ao-PWV), and albuminuria are independent predictors for cardiovascular disease in type 2 diabetes mellitus (T2DM). Whether angiotensin receptor blockers (ARBs), drugs with cardio-renal protective effects, improve Ao-PWV to a greater extent than other equipotent antihypertensive medications remains unclear. After a 4-week washout phase, we compared the effects of valsartan (n=66), an ARB, with that of amlodipine (n=65), a calcium channel blocker on Ao-PWV in 131 T2DM patients with pulse pressure (PP) >or=60 mm Hg and raised albumin excretion rate (AER) in a 24-week randomized, double-blind, parallel group study. Hydrochlorothiazide (HCTZ) 25 mg/d was added to valsartan 160 mg and amlodipine 5 mg/od uptitrated to 10 mg/od after 4 weeks to ensure equivalent BP control. After 24 weeks brachial and central aortic PP had fallen to a similar extent with attained mean (SD) brachial and central PP of 61.6 (13.6) and 47.3 (14.1) mm Hg in the valsartan/HCTZ group and 61.5 (12.2) and 47.3 (9.9) mm Hg in the amlodipine group, respectively. Ao-PWV showed a significantly greater reduction, mean (95% CI), -0.9 m/s (-1.4 to -0.3) for valsartan/HCTZ compared to amlodipine (P=0.002). AER fell significantly only with Val/HCTZ from 30.8(20.4, 46.5) to 18.2(12.5, 26.3) mcg/min, (P=0.01) with between treatment difference in favor of Val/HCTZ of -15.3mcg/min (P<0.001). Changes in AER and Ao-PWV were not correlated. Valsartan/HCTZ improves arterial stiffness and AER to a significantly greater extent than amlodipine despite similar central and brachial BP control. These 2 effects, which appear independent of each other, may explain the specific cardio-renal protective properties of ARBs.

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Influenza vaccination rates varied widely in patients with heart failure with reduced ejection fraction enrolled in the PARADIGM-HF trial, and vaccination was associated with reduced risk for death, although whether this association was causal cannot be determined.

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In an open-labeled study, 20 elderly, male patients with arterial hypertension (WHO I-II) were treated with the ARB valsartan (80-160 mg once daily) over 8 days. Central retinal artery perfusion at rest and during flicker light stimulation was measured before and after treatment using pulsed wave Doppler sonography. Retinal capillary flow was assessed with scanning laser Doppler flowmetry at rest and following systemic infusion of the nitric oxide synthase (NOS) inhibitor NG-monomethyl-L-arginine (L-NMMA).

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It has been known since the 1990s that long-term morbidity and mortality is improved in patients with heart failure with reduced ejection fraction (HFrEF) by treatments that target the renin-angiotensin-aldosterone system (RAAS). It has also long been thought that enhancement of the activity of natriuretic peptides (NPs) could potentially benefit patients with HFrEF, but multiple attempts to realize this benefit had failed over the years - until 2014, when a large, phase III, randomized, controlled clinical trial (PARADIGM-HF) was completed comparing sacubitril/valsartan with enalapril, a well-established treatment for HFrEF. Sacubitril/valsartan (formerly known as LCZ696) is a first-in-class angiotensin receptor neprilysin inhibitor (ARNI) that simultaneously suppresses RAAS activation through blockade of angiotensin II type 1 receptors and enhances vasoactive peptides including NPs through inhibition of neprilysin, the enzyme responsible for their degradation. In PARADIGM-HF, patients with HFrEF treated with sacubitril/valsartan had 20% less risk for cardiovascular death or hospitalization for heart failure (the primary endpoint), 20% less risk for cardiovascular death, 21% less risk for first hospitalization for heart failure, and 16% less risk for death from any cause, compared with enalapril (all p < 0.001). Concerning tolerability, the sacubitril/valsartan group had higher proportions of patients with hypotension and nonserious angioedema but lower proportions with renal impairment, hyperkalemia, and cough, compared with the enalapril group. The use of sacubitril/valsartan has been endorsed by the latest heart failure treatment guidelines in Europe and the USA. This chapter reviews the discoveries, scientific reasoning, and clinical evidence that led to the development of sacubitril/valsartan, the first novel therapy in a new drug class to improve survival in HFrEF in the last 15 years.

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BP reductions at study end and goal achievement rates were greater with combination therapy (-20/15 mmHg and 72%, respectively) than with either monotherapy (valsartan 160 mg: -14/11 mmHg, 61%; hydrochlorothiazide 25 mg: -14/10 mmHg, 50%) for the overall population (N=1313) and in patient subgroups. Patients treated with initial combination therapy reached goal in 27-56% of the time needed for those treated with monotherapy. Combination therapy was well tolerated and was associated with a decreased incidence of hypokalemia compared with hydrochlorothiazide monotherapy.

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Valsartan has been reported to have the function of treating hypertension and improving the prognosis of patients. Many studies indicated that valsartan can also increase angiotensin II, andosterone and plasma renin activity (PRA). Autoantibodies against the angiotensin II type 1 receptor (AT1-AA) have been showed to increase reactive oxygen species (ROS) and calcium (Ca2+) and result in apoptosis in vascular smooth muscle cells. In this study, we attempted to explore the effect of valsartan on AT1-AA-induced apoptosis in endothelial progenitor cells.

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The LVSP and +dp/dt(max) of the control group were significantly higher than the other 4 groups (all P < 0.01). The LVSP and +dp/dt(max) of the valsartan group were significantly higher than those of the I/R group (both P < 0.01). The LVSP and +dp/dtmax of the valsartan + HOE140 group were significantly lower than those of the valsartan group (P < 0.01 and P < 0.05). The no-flow area of the HOE140 group was not significantly different from that of the I/R group (P > 0.05). The no-flow area of the valsartan group was significantly smaller than that of the I/R group, almost half of that of the latter (P < 0.01). The CK-MB levels after I/R at different time points were all significantly higher than that of the control group (all P < 0.01). The CK-MB levels of the HOE140 group were not significantly different from those of the I/R group (all P > 0.05). The CK-MB levels at different time-pints of the valsartan group were all significantly lower than those of the I/R group (all P < 0.01). The CK-MB levels at different time-pints of reperfusion of the valsartan + HOE140 group were all significantly higher than those of the valsartan group (all P < 0.05). Linear correlation analysis showed that the CK-MB level 60 minutes after reperfusion was positively correlated with the no-flow area with a correlation coefficient of 0.85 (P < 0.01).

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Effects of the angiotensin II type 1 (AT1) receptor antagonist valsartan and the angiotensin-converting enzyme (ACE) inhibitor enalapril were studied in streptozotocine (STZ)-induced diabetes in rats on the basis of microalbuminuria (Ma) and renal morphology. Five groups of Wistar rats were used, one group was the non-diabetic control, one group consisted of untreated STZ-diabetics and 3 groups of STZ-diabetics were treated with either enalapril and/or valsartan for 30 days. Blood glucose (BG) and Ma levels, body and kidney weight and glomerular size were measured. Immunohistochemical staining with an anti-transforming growth factor-beta1 (TGF-beta1) antibody was performed as well. In STZ-diabetics, BG and Ma levels were significantly increased when compared with the non-diabetic group. Although Ma levels in the valsartan-treated group was found to be higher than those in the non-diabetics group after 15 days of treatment, in all treated diabetic groups Ma levels were significantly decreased as compared with STZ-diabetics at the end of the experiment. Thickening of the glomerular and tubular basement membranes, increased mesangial matrix and glomerular size were found in the untreated diabetic group. All these changes were less in the treated groups. A significant increase in TGF-beta1 immunoreactivity was found in glomeruli of untreated STZ-diabetics as compared with non-diabetics. Again, TGF-beta1 expression was decreased in the treated groups as compared with untreated STZ-diabetics. We conclude that valsartan and enalapril have renoprotective effects in diabetic nephropathy. A combined therapy has an advantage because lower dosages of these drugs can be used. Their beneficial effects are related to a blockade of the renin-angiotensin system (RAS) and a decrease in TGF-beta1 expression in glomeruli.

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Subgroup analyses were performed for the diabetic and nondiabetic cohorts from 3 randomized clinical trials that had evaluated the systolic blood pressure (SBP)-lowering efficacy and tolerability of an angiotensin receptor blocker, valsartan, alone or in combination with hydrochlorothiazide to determine when and how to initiate combination therapy in hypertensive patients with diabetes. Blood pressure reductions achieved with monotherapy were compared with combination therapy in the diabetic and nondiabetic cohorts. In addition, multivariate models were developed to predict the likelihood of the goal SBP of < 130 mm Hg being reached in a diabetic patient with monotherapy or combination therapy across the range of baseline SBP values. In 2 of the 3 trials, comparable reductions in SBP were seen in the diabetic and nondiabetic cohorts. In all 3 studies, however, combination therapy provided greater blood pressure-lowering efficacy than monotherapy. The probability of achieving goal SBP was greater for diabetic patients started on combination therapy compared with monotherapy.

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This observation suggests that although angiotensin receptor antagonists do not affect prostaglandin metabolism, the administration of a non-steroidal anti-inflammatory drug blunts the natriuretic response to angiotensin receptor blockade.

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Renin-angiotensin system inhibitors transiently induce apoptosis at the onset of cardiac hypertrophy regression in spontaneously hypertensive rats (SHRs). The focus of this study is to evaluate the cell selectivity of this response.

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Valsartan is a highly selective angiotensin II AT1-receptor antagonist for the treatment of hypertension. Valsartan is mainly excreted into the bile in unchanged form. Because valsartan has an anionic carboxyl group, we hypothesized that a series of organic anion transporters could be involved in its hepatic clearance. In this study, to identify transporters that mediate the hepatic uptake and biliary excretion of valsartan and estimate the contribution of each transporter to the overall hepatic uptake and efflux, we characterized its transport using transporter-expressing systems, human cryopreserved hepatocytes, and Mrp2-deficient Eisai hyperbilirubinemic rats (EHBRs). Valsartan was significantly taken up into organic anion-transporting polypeptide (OATP) 1B1 (OATP2/OATP-C)- and OATP1B3 (OATP8)-expressing HEK293 cells. We also observed saturable uptake into human hepatocytes. Based on our estimation, the relative contribution of OATP1B1 to the uptake of valsartan in human hepatocytes depends on the batch, ranging from 20 to 70%. Regarding efflux transporters, the ratio of basal-to-apical transcellular transport of valsartan to that in the opposite direction in OATP1B1/MRP2 (multidrug resistance-associated protein 2) double transfected cells was the highest among the three kinds of double transfectants, OATP1B1/MRP2, OATP1B1/multi-drug resistance 1, and OATP1B1/breast cancer resistance protein-expressing MDCKII cells. We observed saturable ATP-dependent transport into membrane vesicles expressing human MRP2. We also found that the elimination of intravenously administered valsartan from plasma was markedly delayed, and the biliary excretion was severely impaired in EHBR compared with normal Sprague-Dawley rats. These results suggest that OATP1B1 and OATP1B3 as the uptake transporters and MRP2 as the efflux transporter are responsible for the efficient hepatobiliary transport of valsartan.

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Telmisartan, but not valsartan, inhibits HASMCs proliferation and has dose-dependent response without stimulation of AngII. AT2 receptor up-regulation of telmisartan contributes to its greater antiproliferative effects than valsartan. Its PPAR-γ activation does not play a critical role in inhibiting HASMCs proliferation.

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Co-amorphization has recently been shown to be a promising approach for stabilizing amorphous drugs and improving the dissolution rate of poorly water-soluble drugs. In this study, three basic amino acids were chosen as small molecular weight excipients to interact with the drug to form co-amorphous combinations. The co-amorphous combinations of valsartan (VAL) with l-histidine, l-arginine, and l-lysine were prepared by vibrational ball milling. Solid-state characterization with X-ray powder diffraction and differential scanning calorimetry (DSC) revealed that all of the co-amorphous mixtures were homogeneous. The molecular interactions of the co-amorphous mixtures were investigated through the glass transition temperature (Tg) in the DSC measurements and Fourier transform infrared spectroscopy. The drug remained chemically stable during the milling process, and the co-amorphous formulations were generally physically stable over at least 3 months at 40 °C under dry conditions. The dissolution rate of all of the co-amorphous mixtures was significantly increased over that of the amorphous VAL alone. The results of this study demonstrated the potential of amino acids as small molecular weight excipients in co-amorphous formulations to improve the drug solubility and dissolution rate.

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Biologically active natriuretic peptides (NPs) are an integral part of cardiac homeostasis as they help to maintain sodium and fluid balance. When homeostasis is perturbed by neurohormonal activation in heart failure, levels of NPs rise in response. Neprilysin (NEP) is a naturally occuring enzyme that breaks down NPs. Scientists have recently discovered a novel pharmacologic agent that combines a NEP inhibitor and an angiotensin receptor blocker. In a large clinical trial, this new drug was found to reduce hospitalization and mortality in systolic heart failure. The challenges of implementing this therapy include patient selection, cost, and risk of side effects including angioedema and Alzheimer's disease.

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A reliable, simple, and robust liquid chromatography-tandem mass spectro-metric (LC-MS/MS) method has been developed and validated that employs solid-phase extraction for the simultaneous estimation of amlodipine and valsartan in human K3EDTA plasma using amlodipine-d4 and valsartan-d9 as internal standards. Chromatographic separation of amlodipine and valsartan was achieved on the Luna C18 (2)100A (150 × 4.6 mm, 5 μm) column using acetonitrile: 5 mM ammonium formate solution (80:20, v/v) as the mobile phase at a flow rate of 0.8 mL/min in isocratic mode. Quantification was achieved using an electrospray ion interface operating in positive mode, under multiple reaction monitoring (MRM) conditions. The assay was found to be linear over the range of 0.302-20.725 ng/mL for amlodipine and 6.062-18060.792 ng/mL for valsartan. The method has shown good reproducibility, as intra- and interday precisions were within 10% and accuracies were within 8% of nominal values for both analytes. The method was successfully applied for the bioequivalence study of amlodipine and valsartan after oral administration of a fixed dose of the combination. Additionally, as required by the current regulatory bodies, incurred sample reanalysis was performed and found to be acceptable.

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60 patients (39 men and 21 women, mean age 63.9 ± 10.8 years, P > 140/90 mmHg with a background of combined antihypertensive therapy) were involved in the study. Valsartan (Valsacor®) was added to the standard therapy. The follow-up continued for three months, with clinical visits at initiation and completion of the study. The echocardiographic (EchoCG) evaluation included measurements of left ventricular and left atrial dimensions and function via longitudinal strain and Doppler-analysis of the transmitral blood flow.

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A simple, sensitive, rapid, and reproducible analytical method of manassantin B in rat plasma by high performance liquid chromatography with fluorescence detection (HPLC-FL) was developed for its application to pharmacokinetic study in rats. Valsartan (VST) was used as an internal standard (IS) in this quantitative analytical method. Manassantin B and VST were extracted by simple and efficient protein precipitation method. Manassantin B was detected at 282/322nm (excitation/emission) wavelengths using FL detector. The chromatographic separation was obtained with reverse phase C18 column and the mobile phase composed of potassium phosphate buffer containing 0.025% trifluoroacetic acid (pH 2.5; 5mM) and acetonitrile including 0.025% trifluoroacetic acid (20:80, v/v) at 1.0mL/min flow rate. The linearity was established at 25.0-10000ng/mL and the lower limit of detection (LLOD) was 7ng/mL. The intra- and inter-day accuracy and precision values of manassantin B were within±15% of the theroretical values and <9% from the nominal concentrations, respectively. Accuracy and precision values of manassantin B after stability tests were also within the acceptable ranges. Developed assay was also successfully applied to pharmacokinetic study after intravenous administration of manassantin B in rats.

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The VF-HT-AF study is a multicenter, randomized, open-label, four-arm parallel group study with comparative evaluation of valsartan and fluvastatin as upstream therapies for the treatment of non-permanent AF complicated by hypertension. The primary outcome measure is change in the development of paroxysmal AF into persistent or permanent AF, the development of persistent AF to permanent AF, and change in incidence of overall and persistent AF recurrence, as evaluated by 7-days ambulatory electrocardiograph monitoring (Holter) and patients' diaries during 2 years' follow-up. Secondary outcome measures of this study include the occurrence of: (1) fatal and nonfatal myocardial infarction; (2) heart failure (New York Heart Association stage III or IV); (3) cardiogenic shock; (4) serious bleeding necessitating hospitalization; (5) malignant ventricular arrhythmia; (6) revascularization therapy; (7) radiofrequency catheter ablation of AF; (8) changes of left atrial dimension, as measured by ultrasound echocardiography; (9) stroke; (10) cardiovascular mortality; and (11) all-cause mortality. A total of 1879 patients will be investigated from 15 medical centers throughout China to obtain the relevant information.

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Angiotensin II receptor blockade has been shown to have a beneficial effect on the angiopathies of hypertension and hyperglycemia in patients with type 2 diabetes. However, the effect of angiotensin II receptor blockade on monocyte and endothelial cell adhesion markers in type 2 diabetes is poorly understood. We investigated the effects of valsartan on these markers in 53 hypertensive patients with and without type 2 diabetes mellitus. Levels of monocyte activation markers (soluble CD14: 2.1+/-0.9 vs. 3.3+/-1.4 microg/ml, p<0.01; monocyte chemotactic peptide: 392+/-94 vs. 489+/-114 pg/ml, p<0.05; and monocyte-derived microparticles: 264+/-98 vs. 511+/-128/microL, p<0.01) and endothelial cell activation markers (soluble E-selectin: 41+/-11 vs. 61+/-20 ng/ml, p<0.001; and soluble vascular cell adhesion molecule-1: 478+/-82 vs. 584+/-101 ng/ml, p<0.01) were significantly increased in hypertensive patients with type 2 diabetes compared to normotensive controls. In addition, the concentrations of adiponectin were significantly decreased in patients with type 2 diabetes (8.1+/-3.1 vs. 5.2+/-2.5 microg/ml, p<0.01). Regardless of the presence of diabetic complications, both systolic and diastolic blood pressures significantly decreased after valsartan administration (valsartan 80 mg/day for 8 weeks). Monocyte and endothelial cell activation markers were decreased significantly in patients with type 2 diabetes after valsartan treatment, but not in non-type 2 diabetic patients. In addition, valsartan alleviated hypoadiponectinemia in hypertensive patients with diabetes (before vs. after: 5.2+/-2.5 vs. 7.6+/-2.7 microg/ml, p<0.001) but did not increase adiponectin levels in the non-diabetic hypertensive group, for which the average adiponectin level was normal prior to treatment. These results suggest angiotensin II receptor blockade (valsartan) may be beneficial as an anti-atherosclerotic therapy in patients with type 2 diabetes in addition to its anti-hypertensive action.

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Thirty-six pigs were assigned randomly to placebo, enalaprilat or valsartan groups. After a 30-min period of stabilization following anaesthesia and injection of the study drug, the animals were bled in two equal steps of 20% of their estimated blood volume (20% BV and 40% BV).

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In SHR diastolic dysfunction was accompanied by concentric hypertrophy,cardiac oxidation, a reduction in cardiac BH4 and NO production. Administered with BH4 and Valsartan for four weeks, the data showed that both can reverse hypertrophy and improve diastolic function.BH4 and Valsartan blunted the expression of hypertrophy markers α-skeletal actin (α-SA) and β-myosin heavy chain (β-MHC), only BH4 reduced hypertension induced myocardial fibrosis and expression of transforming growth factor-β1(TGF-β1). BH4 reduced cardiac oxidant stress and increased NO production. Exogenous BH4 increased the phosphorylated Akt level and enhanced expression of Bcl-2.

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diovan generic brand 2015-10-29

Left ventricular (LV) dysfunction and/or heart failure (HF) are frequent complications of hypertension and myocardial infarction (MI), placing affected patients at increased risk of significant morbidity and premature death. Given that the renin-angiotensin-aldosterone system (RAAS) is activated and of pathophysiological importance in such patients, a strong therapeutic rationale exists to target the main effector mechanism (that is, angiotensin II [Ang II]) in order to lessen the associated morbidity and mortality burden. Angiotensin-converting enzyme (ACE) inhibitors have been shown to reduce mortality and LV dysfunction and to slow disease progression in patients with HF, including high-risk, post-MI patients. However, ACE inhibitors (ACE-Is) may not provide optimal long-term RAAS blockade (a finding that is associated with a worse prognosis) and many patients are unable to tolerate such therapy (because of troublesome dry cough, for example). In contrast, Ang II receptor blockers (ARBs) may block the RAAS more completely than ACE-Is and appear to be better tolerated. Several large-scale trials gave evaluated the efficacy of ARBs in patients with LV buy diovan dysfunction and/or HF (including high-risk, post-MI patients), and have confirmed their utility as an efficacious and well-tolerated alternative to ACE-Is in this setting.

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Val with or without Ben remarkably decreased SBP and DBP in patients with essential hypertension within 6 weeks. Antihypertensive efficacy was weakened after buy diovan long-term use of Val alone. The antihypertensive effect of Val+Ben group was the most remarkable among 3 groups and could avoid the side effects of high plasma Ang II.

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The angiotensin receptor blockers (ARBs) are very effective and safe antihypertensive drugs. They exert their antihypertensive effect through buy diovan blockage of the angiotensin II, type 1 receptor and quite possibly through stimulation by angiotensin II of the unoccupied type 2 receptor. Besides hypertension, the ARBs have been found recently to be of value in the treatment of heart failure and diabetic nephropathy. In addition, ARBs have emerged lately as being very effective and perhaps superior to other antihypertensive drugs in the prevention of de novo or recurrent strokes. Other actions that may account for their stroke-protective effects include their antiatherogenic, antidiabetic, antiplatelet aggregating, hypouricemic, and atrial antifibrillatory actions. All these actions make the ARBs a true pleiotropic class of drugs. Each of the foregoing effects will be discussed briefly in this concise review.

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The VALUE trial was a randomised-controlled, double-masked investigation of valsartan versus amlodipine in patients buy diovan 50 years or older with hypertension and high risk of cardiovascular events. Mean follow-up time was 4.2 years. We calculated the standard deviation (SD) of mean systolic blood pressure from visits from 6 months onward, excluding patients with less than 2 visits, or stroke or cardiac events during the first 6 months. In the pooled treatment arms, we grouped SD in quintiles and compared the risk of stroke or cardiac events in the highest and the lowest quintile, using a Cox regression model, adjusting for a number of prognostic variables, including randomised treatment and mean BP from 6 months onwards.

diovan 40mg tablet 2017-08-14

One hundred sixty-eight adult outpatients with mild to moderate hypertension were buy diovan randomly allocated in double-blind fashion and equal number to receive 80 mg valsartan or 5 mg amlodipine for 12 weeks. After 8 weeks of therapy, in patients whose blood pressure remained uncontrolled, 5 mg amlodipine was added to the initial therapy. Patients were assessed at 4, 8, and 12 weeks. The primary efficacy variable was change from baseline in mean sitting diastolic blood pressure at 8 weeks. Secondary variables included change in sitting systolic blood pressure and responder rates.

diovan generic picture 2015-10-12

This study aimed to improve the pH-independent solubility and dissolution characteristics of valsartan via the preparation of solid dispersions (SD) with poloxamer 407. SDs was prepared by using the solvent method at various drug-polymer ratios and their dissolution characteristics were examined at different pHs. Oral pharmacokinetics of SDs was also evaluated in rats. Compared to the untreated powder, SDs significantly improved the dissolution rate as well as the extent of drug release at low pH. Particularly, SD having the drug-polymer ratio of 1:5 exhibited pH-independent dissolution of valsartan, resulting in the rapid and complete drug release over the pH range of 1.2 to 6.8. The improved dissolution of valsartan via SD formulation appeared to be well correlated with the enhanced oral exposure of valsartan in rats. SDs increased C(max) and AUC(0-24) of valsartan by 2-7 folds in rats, implying that SDs buy diovan should be effective to improve the bioavailability of valsartan. In conclusion, SDs containing poloxamer 407 appeared to be effective to improve the pH-independent dissolution and oral absorption of valsartan.

diovan 600 mg 2016-11-07

It is evident from this study that the gel formulation buy diovan of ultradeformable vesicles of valsartan is a promising delivery system for lipophilic drugs, and has reasonably good stability characteristics.

diovan tab 2015-05-14

Twelve-week-old male Wistar rats and spontaneously hypertensive rats (SHRs) were anesthetized with urethane, and underwent real-time cystometry and blood pressure monitoring. The SHRs were administered nifedipine or valsartan intravenously. The Wistar rats were administered intravenous noradrenaline continuously. The intercontraction intervals, maximum detrusor pressures, blood pressure during the voiding and the urine storage phases, blood pressure elevations associated with the buy diovan VVRs, and arterial pulses were assessed. Plasma adrenaline and noradrenaline concentrations were measured using HPLC. The degree of atherosclerosis was assessed histologically based on the aortic wall thickness.

diovan 90 mg 2015-02-16

Renal interstitial fluid angiotensin II significantly increased after development of diabetes. In contrast, basal renal interstitial fluid nitric oxide decreased significantly over 12 weeks after development of diabetes. Both losartan and valsartan caused a further increase in renal angiotensin II levels. Some 4 h after buy diovan administration, there was significantly greater increase in renal nitric oxide after administration of valsartan than of losartan. At 8 h post- treatment, only valsartan caused a significant increase in renal nitric oxide levels.

diovan 80mg tablets 2015-06-23

Ischemia was induced buy diovan by partial ligation of the left common iliac artery.

diovan hct tablets 2016-04-26

The addition of an angiotensin II receptor blocker to calcium channel blocker-based antihypertensive therapy may be associated with enhanced efficacy and reduced risk of adverse buy diovan events.

diovan 360 mg 2015-03-09

Amlodipine/valsartan/hydrochlorothiazide (HCTZ) is a fixed-dose combination of the well established antihypertensive agents amlodipine (a calcium channel antagonist), valsartan (an angiotensin II receptor antagonist), and HCTZ (a thiazide diuretic). In patients with moderate or severe hypertension, triple combination therapy with amlodipine + valsartan + HCTZ produced significantly greater reductions from baseline in mean sitting systolic and diastolic BP (msSBP and msDBP) than either valsartan + HCTZ, amlodipine + HCTZ, or amlodipine + valsartan in a large, 8-week, randomized, double-blind, multinational, phase III trial. Furthermore, the proportion of patients achieving overall BP control at endpoint was significantly greater with the triple combination regimen than with any of the dual regimens, with significantly more triple combination recipients achieving msSBP and msDBP control at each assessment throughout the trial. Subgroup analyses of this study suggested that amlodipine + valsartan + HCTZ was generally more effective buy diovan in reducing BP and providing overall BP control than the dual combination therapies, irrespective of age, race, gender, ethnicity, or hypertension severity. Several smaller studies provide data that support the efficacy of amlodipine + valsartan + HCTZ in patients whose BP is inadequately controlled with amlodipine + valsartan, amlodipine + HCTZ, or valsartan + HCTZ dual combination therapy. Treatment with amlodipine + valsartan + HCTZ for up to 8 weeks was generally well tolerated in the large, phase III trial, with most adverse events being transient and of mild to moderate severity.

diovan tab 80mg 2015-04-29

AGTR1 expression is potentially associated with airway remodeling buy diovan and dysfunction in asthma. Ang II and AGTR1 may participate in airway inflammation and airway remodeling of chronic antigen-exposed rats. Valsartan, a AGTR1 antagonist, could inhibit AGTR1 expression and partially inhibits structural airway changes as well as airway inflammation in chronic OVA-exposed rats.

co diovan dosage 2017-07-10

All patients were buy diovan treated during four 6 week periods, in random order, with angiotensin receptor blockade (valsartan 320 mg/day) or placebo, each combined with, consecutively, a low sodium diet (target 50 mmol Na(+)/day) and a regular sodium diet (target 200 mmol Na(+)/day), with a background of ACE inhibition (lisinopril 40 mg/day) during the entire study. The drug interventions were double blind; the dietary interventions were open label.

diovan hct dosage 2016-06-14

Recent studies have demonstrated the presence of the (pro)renin receptor (PRR) in the glomerular mesangium and the subendothelial layer of the renal arteries. We hypothesized that diabetes upregulates PRR expression through enhanced angiotensin subtype 1 (AT1) receptor-NADPH oxidase cascade activity. Using real-time polymerase chain reaction, Western blot analysis and immunostaining, we studied renal localization of the PRR in the streptozotocin-induced diabetic rat model and in response to 1 week of treatment with the AT1 receptor blocker valsartan (10 mg kg(-1) day(-1)), the angiotensin AT2 receptor blocker PD123319 (0.5 mg kg(-1) day(-1)) or the NADPH oxidase inhibitor diphenylene Voltaren 45 Mg iodonium (DPI; 0.5 mg kg(-1) day(-1)) 6 weeks post-induction of diabetes. Both PRR mRNA and protein were expressed constitutively in the kidneys of normal rat renal cortex and medulla, mainly in glomerular mesangium, proximal, distal and collecting tubules. Compared with normal rats (100%), diabetic rats demonstrated an increase in renal PRR mRNA (184%), protein (228%) and immunostaining. Valsartan and DPI prevented the increase in the PRR mRNA (106 and 126%, respectively), protein (97 and 140%, respectively) and immunostaining that was seen in the kidneys of diabetic rats. The AT2 blocker PD123319 did not have significant effects on PRR mRNA (157%) or protein expression (200%) in the kidneys of diabetic rats. These results demonstrate that the PRR is constitutively expressed in renal glomeruli and tubules. Expression of the PRR is upregulated in diabetes via enhancement of AT1 receptor-NADPH oxidase activity.

diovan dosage amounts 2016-09-20

Aml/Val SPC was effective for BP reductions and well tolerated in hypertensive patients, not adequately controlled by monotherapy, in Periactin Drug Information a daily clinical setting in Indonesia.

diovan cost 2015-06-16

Bosentan and valsartan acted complementarily, and co-treatment with both drugs had an additive protective effect Propecia 2 Mg against renal fibrosis.

diovan water pill 2017-06-16

Aliskiren is an orally administered, nonpeptide direct renin inhibitor indicated for the management of hypertension. Aliskiren was effective in controlling blood pressure (BP) as monotherapy and in combination with other antihypertensives, in large, randomized trials. Aliskiren 150-300 mg/day as monotherapy was effective in lowering BP across short- (≤12 weeks) and longer-term (up to 54 weeks) periods, providing sustained and consistent effects with 24-hour BP control. Compared with other antihypertensives, aliskiren was generally as effective as hydrochlorothiazide (HCTZ), valsartan, losartan, irbesartan and lisinopril in reducing BP. Furthermore, short-term aliskiren was noninferior to ramipril in reducing BP, but with a longer treatment duration, a greater efficacy of aliskiren-based therapy over ramipril-based therapy was demonstrated. Additional BP-lowering effects occurred when aliskiren was coadministered (as a fixed-dose combination or separate tablets) with other antihypertensives, including HCTZ, valsartan and amlodipine, according to large, randomized trials of short- (≤12 weeks) and longer-term (up to 54 weeks) duration. Combination therapy with aliskiren plus HCTZ was effective in hypertensive patients when administered as initial therapy or to patients previously treated with HCTZ or aliskiren monotherapy. Aliskiren-based Strattera Open Capsules therapy was also effective in lowering BP in obese patients, patients with type 1 or 2 diabetes mellitus, patients with metabolic syndrome and the elderly. Aliskiren efficacy was observed irrespective of patient age, sex or ethnicity. Aliskiren monotherapy or combination therapy was generally well tolerated over short- and longer-term study durations in large, randomized clinical trials. Clinical trials to evaluate the effects of aliskiren on clinical outcomes, including renoprotective and cardioprotective effects, are currently ongoing. Thus, aliskiren is a useful option for the treatment of patients with stage 1 to stage 2 (mild to moderate) hypertension, alone or in combination with other antihypertensives, including HCTZ, valsartan or amlodipine.

diovan equivalent drugs 2017-01-17

In 5010 heart failure patients on background therapy and randomized Naprosyn Generic to valsartan and placebo, serial recordings of left ventricular internal diastolic diameter (LVIDd) and ejection fraction (EF) were read at sites that had to meet qualifying standards before participating. Baseline LVIDd and EF were pooled across treatments and retrospectively grouped by quartiles Q1 to Q4, representing best to worst. Kaplan-Meier survival curves were obtained by the log-rank test. Q1 was compared with Q4 for mortality and combined mortality and morbidity (M + M) from Cox regression risk ratios (RRs). Valsartan versus placebo changes from baseline in LVIDd and EF were analyzed by quartiles from analysis of covariance. Valsartan and placebo were compared by RRs for M + M.

diovan generic valsartan 2016-07-25

Pue attenuates Ang II-induced cardiac hypertrophy by inhibiting activation of the redox-sensitive ERK1 Neurontin Yellow Pill /2, p38 and the NF-κB pathways.

diovan tablet 80mg 2016-02-15

VALID is a multicenter collaborative study to evaluate the impact of dose of valsartan on the post-MI ventricular remodeling. The results of the study provide information about optimal dosing of the drug in the management of patients after MI. The results will be available by 2012.

diovan generic equivalent 2015-06-14

Twenty-seven stable cardiac transplant recipients were randomized to remain on ACE inhibitor therapy (n = 8) or to receive valsartan (n = 19). Two additional endomyocardial biopsy samples were obtained at baseline and after 9 months of therapy. The expression of cardiac angiotensin type I and II receptors and atrial natriuretic factor (ANF) was measured by quantitative polymerase chain reaction. The expression and phosphorylation levels of selected signal transduction pathways were analyzed by immunoblotting.

diovan dosage times 2016-12-13

Valsartan is a specific angiotensin II receptor antagonist with high selectivity for the AT(1) receptor subtype. After oral administration of single or repeated once-daily doses, valsartan 40-80 mg inhibits the pressor response to angiotensin II for 24 hours. In patients with mild-to-moderate hypertension, efficacy of valsartan appears to be independent of age, sex, and race, and is at least equivalent to that of calcium antagonists, ACE inhibitors, or thiazide diuretics. Response rate to valsartan 160 mg o.d. is significantly greater than after receiving losartan 100 mg o.d. Valsartan has additive effects with other antihypertensive drugs and combination therapy is effective in severe hypertension and in hypertension with renal insufficiency, where renal function is well maintained. Valsartan has good tolerability with a side-effect profile indistinguishable from placebo and superior to that of comparable drugs. Valsartan does not cause cough or adverse metabolic effects; first dose hypotension and rebound hypertension on abrupt withdrawal have not been encountered. Valsartan has clear clinical advantage in the management of hypertension. Its impact on prognosis in patients with a high risk of cardiovascular morbidity and mortality is under evaluation.

diovan mg 2017-04-29

This multicenter, double-blind, parallel group, forced-titration study of individuals with stage 2 hypertension, compared the efficacy of valsartan and amlodipine in combination with HCTZ on ABP reduction.

generic diovan reviews 2017-08-15

We prospectively studied 95 hypertensive patients with diabetes mellitus. Patients were treated with candesartan (8 mg/day, n = 47) or valsartan (80 mg/day, n = 48) for 15 months. Blood pressure (BP), urinary albumin excretion (UAE), biochemical markers, plasma aldosterone concentration (PAC), and plasma renin activity (PRA) were measured before and at 3, 6, 12, and 15 months of treatment. Nine patients who exhibited aldosterone breakthrough after treatment with ARB were placed on spironolactone (25 mg/day) for 3 months, and BP, UAE, and biochemical markers were measured after treatment.

diovan overdose deaths 2017-01-12

An observational case series with data collected retrospectively from eight PICs in Austria, Germany and Switzerland. Inclusion criteria were monoexposure, defined dose, and documented follow-up.