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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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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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This was a multi-centre, randomised, double-blind, active-controlled study in patients with essential hypertension. After a washout period followed by a single-blind amlodipine 10 mg run-in period, patients with mean sitting diastolic blood pressure (msDBP) > or =90 mmHg and <110 mmHg were randomised to receive amlodipine/valsartan (10/160 mg o.d.) or amlodipine (10 mg o.d.) for 8 weeks.

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The effect of ramipril or valsartan on peritubular capillaries was investigated in a remnant kidney model using male Sprague-Dawley rats sacrificed post-operatively at 3, 6 and 12 weeks respectively. Peritubular capillaries and tubulointerstitial hypoxia in untreated remnant kidney rats (n = 26), remnant kidney rats treated with ramipril (n = 22, 0.5 mg/kg/day), valsartan (n = 22, 30 mg/kg/day) or amlodipine (n = 22, 30 mg/kg/day) and sham-operated rats (n = 22) were assessed by CD141 and HIF-1alpha staining.

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Angiotensin II receptor blockers (ARBs) are the most recent class of anti-hypertensive drug to enter clinical use for chronic heart failure (CHF). In the landmark Valsartan Heart Failure Trial (Val-HeFT), valsartan reduced the risk of the combined endpoint of all-cause mortality and morbidity by 13.2% over a 2-year follow-up. Although it significantly improved a pre-specified primary endpoint, it did not improve the endpoint of all-cause mortality. Valsartan administered to patients not receiving angiotensin-converting enzyme inhibitors (ACEI) at baseline reduced the endpoint of all-cause mortality by 33% and the combined endpoint of mortality and morbidity by 44%, compared with placebo. Based on these findings, valsartan became the first ARB to be approved by the US Food and Drug Administration for the treatment of New York Heart Association class II-IV HF in patients who are intolerant of ACEIs. This review provides a summary of the key Val-HeFT results and their implications in the treatment of CHF patients.

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Using radiotelemetry combined with spectral analysis with a fast Fourier transformation algorithm, we compared the effects of various doses of telmisartan and valsartan on BP and its variability during dark (active phase) and light (inactive phase) periods over 5 weeks in SHR/NDmcr-cp(+/+)(SHRcp) rats, a model of metabolic syndrome. We also compared the effects of these ARBs on autonomic nervous system, central oxidative stress, and inflammation in SHRcp rats.

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A 47-year-old man admitted with diffuse, itchy erythematous maculopapular eruption all over the body. He has been taking 160 mg valsartan daily for 10 days before onset of the eruption. On the third day of valsartan therapy, erythema had appeared over the face and spread throughout the whole body within a week. Histopathologic examination of the lesions showed lymphocyte exocytosis, spongiosis, necrotic keratinocytes in the epidermis, and mixed inflammatory cell infiltrates including perivascular eosinophils in the dermis. The patient was diagnosed as drug reaction due to valsartan with historical, clinical and histopathologic features.

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The precise mechanism of salt-induced brain injury is unclear. We examined the detailed causative role of angiotensin II and NADPH oxidase in salt-accelerated brain injury of stroke-prone spontaneously hypertensive rats (SHRSP).

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These results suggest that the cholesterol-independent inhibition of AT1 receptor-mediated VSMC proliferation by statins may contribute to the beneficial effects of statins combined with an ARB on vascular diseases.

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Despite a shorter half-life, 160 mg/day valsartan was more effective in lowering blood pressure over 24 h than 80 mg/day telmisartan. Furthermore, valsartan was also more effective in lowering arterial pulse pressure, an observation that may have important therapeutic implications, given the mounting evidence that pulse pressure may be a risk factor for future cardiovascular events.

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To compare valsartan with other commonly used antihypertensives in a National multicentric study.

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We conducted an open-label, randomized trial to compare the effects of aliskiren with those of valsartan. Patients with BP <150/90 mmHg, an estimated glomerular filtration rate of 90-30 mL/min/1.73 m(2), and albuminuria >30 mg/g, despite treatment with a 160 mg daily dose of valsartan, were randomly assigned to the following two groups: the aliskiren group, who switched from 160 mg/day valsartan to 150 mg/day aliskiren, which was later increased to 300 mg/day (n = 20); and the valsartan group, who continued with 160 mg/day valsartan (n = 20).

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The strategy of initiating hypertension treatment with combination versus single-drug therapy was formally tested in a prospective, double-blind, parallel-group trial in blacks with stage 2 hypertension (mean sitting systolic BP (MSSBP) >or=160 and <200 mm Hg). Participants were randomized equally to amlodipine/valsartan (A/V) (n=286) or amlodipine (A) monotherapy (n=286). After 2 weeks, there was forced titration of A/V 5/160 mg to A/V 10/160 mg and of A 5 to A 10 mg followed by 10 additional weeks of treatment. If SBP was >or=130 mm Hg at week 4, the protocol allowed optional titration of A/V to the 10/320 mg dose and, at week 8, hydrochlorothiazide 12.5 mg was optionally added to both A/V and A if SBP >or=130 mm Hg. Amlodipine/valsartan at week 8 lowered MSSBP last observation carried forward significantly>A (33.3 vs 26.6 mm Hg, P<0.0001). Lowering of MSSBP with A/V significantly exceeded that of A in several specified subgroups-the elderly (>or=65 years), isolated systolic hypertension, and those with body mass index (BMI) >or=30 kg/m(2). More patients treated with A/V than A achieved BP control (<140/90 mm Hg) both at weeks 8 (49.8 vs 30.2%; P<0.0001) and 12 (57.2 vs 35.9%; P<0.0001). Both treatment regimens were well tolerated. In conclusion, the strategy of initiating combination antihypertensive drug therapy in blacks with stage 2 hypertension with amlodipine /valsartan achieves greater and quicker reductions in BP as well as significantly higher BP control rates than starting treatment with amlodipine monotherapy.

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diovan 320 generic 2015-12-02

Fetuin-A (A2-HS-glycoprotein) is a protein that plays several functions in human physiology and pathophysiology. The role of fetuin-A in type 1 diabetes mellitus Imodium Tablets Directions (DM) has been less studied. We investigated the serum levels of fetuin-A in type 1 diabetic patients with microalbuminuria. Furthermore, the blocking effect of renin-angiotensin-aldosteron system on serum levels of fetuin-A was assessed.

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Compared with monotherapy, combination therapy resulted in greater reductions in BP and achievement of goal BP in a shorter period of time. Although interpretation of this study is subject to the limitations associated with any post-hoc analysis, the results suggest that initiating treatment with combination therapy may be considered for expedient and effective BP Singulair Medicine Uses control.

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IS in the control group was 42.9 ± 2.1% of the AR. AL at 25 (21.9 ± 2.9%) and 50 mg/kg/d (15 Suprax Tab .5 ± 1.3%) reduced IS. VA at 16 mg/kg/d (18.8 ± 1.2%), but not at 8 mg/kg/d (35.2 ± 4.0%), limited IS. IS was the smallest in the AL50+VA16 group (6.3 ± 0.9%). Both AL and VA reduced myocardial AT1R levels, without affecting AT2R levels, and increased the expression of Sirt1 and PGC-1α with increased phosphorylation of Akt and eNOS.

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One week after MI, adult male Sprague-Dawley rats were randomized to treatment for 4 weeks with LCZ696 (68 mg/kg body weight perorally; MI-ARNi, n=11) or vehicle (MI-vehicle, n=6). Five weeks after MI, MI-ARNi versus MI-vehicle demonstrated lower LV end-diastolic diameter (by echocardiography; 9.7±0.2 versus 10.5±0.3 mm), higher LV ejection fraction (60± 2 Zithromax Pills 2 versus 47±5%), diastolic wall strain (0.23±0.02 versus 0.13±0.02), and circular strain (-9.8±0.5 versus -7.3±0.5%; all P<0.05). LV pressure-volume loops confirmed improved LV function. Despite similar infarct size, MI-ARNi versus MI-vehicle had lower cardiac weights (P<0.01) and markedly reduced fibrosis in peri-infarct and remote myocardium. Angiotensin II-stimulated incorporation of 3[H]leucine in cardiac myocytes and 3[H]proline in cardiac fibroblast was used to evaluate hypertrophy and fibrosis, respectively. The neprilysin inhibitor component of LCZ696, LBQ657, inhibited hypertrophy but not fibrosis. The angiotensin receptor blocker component of LCZ696, valsartan inhibited both hypertrophy and fibrosis. Dual valsartan+LBQ augmented the inhibitory effects of valsartan and the highest doses completely abrogated angiotensin II-mediated effects.

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Addition of aliskiren, a direct renin inhibitor, to losartan provides additive reduction of urinary albumin excretion in type 2 diabetic patients. However, the detailed effect of aliskiren on type 2 diabetic nephropathy is still unknown. Asacol 800mg Tablets This study was undertaken to examine the efficacy of aliskiren and the combination of aliskiren with valsartan on type 2 diabetic nephropathy.

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Valsartan add-on treatment to improve blood pressure control prevented more cardiovascular events than conventional non-ARB treatment in high-risk hypertensive patients in Japan. These benefits cannot be entirely explained Risperdal Injection Reviews by a difference in blood pressure control.

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In this randomized trial, 293 patients (219 men; mean age, 54.24 [9.77] years) with mild to moderate hypertension were enrolled. After randomization to receive 30-mg fimasartan (n = Periactin Name Brand 115), placebo (n = 117), or 80-mg valsartan (n = 61), the treatment dose was kept constant without dose escalation for 8 weeks. The primary end point was improvement in sitting diastolic blood pressure (SiDBP) from baseline to 8 weeks that was compared between treatments with low-dose fimasartan and placebo. The secondary end point was the overall efficacy and safety of low-dose fimasartan compared with that of placebo or valsartan.

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To explore the potential therapeutic effects of angiotensin(1 Cordarone Reviews -7) (Ang(1-7)), an endogenous ligand of the Mas receptor, on streptozotocin-induced diabetic nephropathy, male Wistar rats were randomly divided into two groups: a control group and a diabetic model group. After 12 weeks, the diabetic rats were divided into subgroups for 4-week treatments consisting of no-treatment group, small-, moderate-, and large-dose Ang(1-7) groups, a valsartan group, a large-dose Ang(1-7) plus valsartan group, and an A779 (antagonist of the Mas receptor) group, each with 15 rats. Ang(1-7) improved renal function, attenuated glomeruli sclerosis, oxidative stress, and cell proliferation, decreased the expression of collagen IV, TGF-β1, VEGF, NOX4, p47phox, PKCα, and PKCβ1, and the phosphorylation of Smad3. In the rat mesangial HBZY-1 cell line, Ang(1-7) decreased high-glucose-induced oxidative stress, the proliferation and expression of NOX4, p47phox, and TGF-β1, the phosphorylation of Smad3, collagen IV, and VEGF, and the membrane translocation of PKCα and PKCβ1. A779 blocked the effects of Ang(1-7) both in vivo and in vitro. The effects of large-dose Ang(1-7) alone and in combination with valsartan were superior to valsartan alone, but the combination had no significant synergistic effect compared with Ang(1-7) alone. Thus, Ang(1-7) ameliorated streptozotocin-induced diabetic renal injury. Large-dose treatment was superior to valsartan in reducing oxidative stress and inhibiting TGFβ1/Smad3- and VEGF-mediated pathways.