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Diovan

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.

Description

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.

Dosage

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.

Overdose

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.

Storage

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.

Contraindications

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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Drugs that block the renin-angiotensin system represent one of the most significant therapeutic interventions available for the treatment of hypertension. The angiotensin II receptor antagonists (AIIRAs), also known as sartans, are one such class of drugs that block the effects of angiotensin II by antagonizing the angiotensin II type 1 receptor. Olmesartan is the newest member of this class.

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among the 120 patients only 109 patients were finally included in the study. Elevenpatients who had had duplicated prescriptionswere excluded from the study. 78% of the patients were on Valsartan for its FDA-approved indications while 22% of patients were for other non-approved indications. Half of the patients were initiated on an ACEi before shifting to Valsartan. The other half of the patients was started with Valsartan as a first line choice without any clinical justification.

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Risk factors for first stroke are well established, but less is known about risk factors for recurrent stroke. In the present analysis, we aimed to assess the effect of heart rate and other possible predictors of stroke in a hypertensive population with previous stroke or transient ischemic attack (TIA).

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A large number of anthropogenic trace contaminants such as pharmaceuticals, their human metabolites and further transformation products (TPs) enter wastewater treatment plants on a daily basis. A mixture of known, expected, and unknown molecules are discharged into the receiving aquatic environment because only partial elimination occurs for many of these chemicals during physical, biological and chemical treatment processes. In this study, an array of LC-MS methods from three collaborating laboratories was applied to detect and identify anthropogenic trace contaminants and their TPs in different waters. Starting with theoretical predictions of TPs, an efficient workflow using the combination of target, suspected-target and non-target strategies for the identification of these TPs in the environment was developed. These techniques and strategies were applied to study anti-hypertensive drugs from the sartan group (i.e., candesartan, eprosartan, irbesartan, olmesartan, and valsartan). Degradation experiments were performed in lab-scale wastewater treatment plants, and a screening workflow including an inter-laboratory approach was used for the identification of transformation products in the effluent samples. Subsequently, newly identified compounds were successfully analyzed in effluents of real wastewater treatment plants and river waters.

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At the end of study, valsartan/HCTZ 80/12.5 mg combination treatment further reduced systolic (-3.5 mm Hg) and diastolic (-2.2 mm Hg) pressures and increased the rate of patients reaching goal BP level (53.9% vs. 40.9%) compared to valsartan 80 mg o.d. monotherapy. Incidence of side effects was similar between the combination therapy and monotherapy groups (8.9% vs. 5.1%, P > 0.05).

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The objective of this study was to investigate the effects of angiotensin II and valsartan, an angiotensin II type 1 receptor (AT1R) blocker, combined with γ-radiation, on vascular endothelial growth factor (VEGF) expression, radiosensitivity, invasive potential, and proliferation activity of nasopharyngeal carcinoma (CNE-2) in vitro. Reverse-transcription PCR and ELISA assayed VEGF expression and secretion in CNE-2 in vitro. Radiosensitization of valsartan on CNE-2 cell in vitro was investigated by a colony-forming assay. The effect of AT1R blocker combined with radiation on invasive potential of CNE-2 cells was evaluated using 24-well Matrigel invasion chambers (Transwell). The apoptosis-inducing effect of valsartan combined with irradiation on apoptosis of CNE-2 was identified by flow cytometry. AT1R was expressed in nasopharyngeal carcinoma cell lines CNE-1 and CNE-2. The expression and secretion of VEGF in CNE-2 could be induced either by angiotensin II or γ-radiation. Furthermore, the suppression of AT1R activation reduced cellular proliferation, invasive potential and resistance to γ-radiation in nasopharyngeal carcinoma cells. In conclusion, AT1R plays a significant role not only in proliferation and invasion, but also in radiation resistance in nasopharyngeal carcinoma cells, the mechanism of which may be involved in the regulation of VEGF expression and secretion.

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db/db mice were treated with aliskiren (3 mg/kg per day), valsartan (5 or 10 mg/kg per day), combined aliskiren (3 mg/kg per day) and valsartan (5 mg/kg per day), and hydralazine (80 mg/kg per day), for 6 weeks, and the protective effects against diabetic nephropathy were compared among each group.

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Valsartan and fluvastatin can reduce myocardial fibrosis, resulting in prevention of left ventricular remodeling and improvement of cardiac function in an experimental model of diabetic cardiomyopathy. The process was related to the inhibition of the overexpression of CTGF and TGFbeta and reduction in cardiac extracellular matrix collagen content. It is also shown that a better result may be obtained with the coadministration of the two drugs than using one alone.

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Tenting area, coaptation depth, annular dilatation, and left atrial size were all associated with the degree of baseline MR. Tenting area was the only significant and independent predictor of worsening MR; a tenting area of 4 cm(2) was a useful cutoff to identify worsening of MR after MI and moderate to severe MR after 20 months.

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Fat1 is an atypical cadherin that controls vascular smooth muscle cell (VSMC) proliferation and migration. Nicotinamide adenine dinucleotide phosphate (NADPH) oxidase 1 (Nox1) is an important source of reactive oxygen species (ROS) in VSMCs. Angiotensin II (Ang II) induces the expression and/or activation of both Fat1 and Nox1 proteins. This study tested the hypothesis that Ang II-induced Fat1 activation and VSMC migration are mediated by Nox1-dependent ROS generation and redox signaling. Studies were performed in cultured VSMCs from Sprague–Dawley rats. Cells were treated with Ang II (1 μmol/L) for short (5 to 30 min) or long term stimulations (3 to 12 h) in the absence or presence of the antioxidant apocynin (10 μmol/L), extracellular-signal-regulated kinases 1/2 (Erk1/2) inhibitor PD98059 (1 μmol/L), or Ang II type 1 receptor (AT1R) valsartan (1 μmol/L). siRNA was used to knockdown Nox1 or Fat1. Cell migration was determined by Boyden chamber assay. Ang II increased Fat1 mRNA and protein levels and promoted Fat1 translocation to the cell membrane, responses that were inhibited by AT1R antagonist and antioxidant treatment. Downregulation of Nox1 inhibited the effects of Ang II on Fat1 protein expression. Nox1 protein induction, ROS generation, and p44/p42 MAPK phosphorylation in response to Ang II were prevented by valsartan and apocynin, and Nox1 siRNA inhibited Ang II-induced ROS generation. Knockdown of Fat1 did not affect Ang II-mediated increases in Nox1 expression or ROS. Inhibition of p44/p42 MAPK phosphorylation by PD98059 abrogated the Ang II-induced increase in Fat1 expression and membrane translocation. Knockdown of Fat1 inhibited Ang II-induced VSMC migration, which was also prevented by valsartan, apocynin, PD98059, and Nox1 siRNA. Our findings indicate that Ang II regulates Fat1 expression and activity and induces Fat1-dependent VSMC migration via activation of AT1R, ERK1/2, and Nox1-derived ROS, suggesting a role for Fat1 downstream of Ang II signaling that leads to vascular remodeling.

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All articles identified from data sources with pertinent information regarding olmesartan medoxomil were evaluated, and all information deemed relevant was included in this review.

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Valsartan (VAL) is an antihypertensive drug marketed in an amorphous form. Amorphous materials can have different physicochemical properties depending on preparation method, thermal history, etc., but the nature of such materials is difficult to study by diffraction techniques. This study characterizes two different amorphous forms of valsartan (AR and AM) using solid-state NMR (SSNMR) as a primary investigation tool, supported by solution-state NMR, FT-IR, TMDSC, and dissolution tests. The two forms are found to be clearly distinct, with a significantly higher level of structural arrangement in the AR form, as observed in (13)C, (15)N, and (1)H SSNMR. (13)C and (15)N NMR indicates that the fully amorphous material (AM) contains an approximately equal ratio of cis-trans conformers about the amide bond, whereas the AR form exists mainly as one conformer, with minor conformational "defects". (1)H ultrafast MAS NMR shows significant differences in the hydrogen bonding involving the tetrazole and acid hydrogens between the two materials, while (15)N NMR shows that both forms exist as a 1,2,3,4-tetrazole tautomer. NMR relaxation times show subtle differences in local and bulk molecular mobility, which can be connected with the glass transition, the stability of the glassy material, and its response to aging. Counterintuitively the fully amorphous material is found to have a significantly lower dissolution rate than the apparently more ordered AR material.

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Valsartan and fosinopril prevent the remodeling of cardiac Zocor Generic Equivalent hypertrophy induced by norepinephrine. Cardiac myocyte apoptosis may play a key role in the heart remodeling.

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Pulmonary damage and fibrosis Generic Ziac Side Effects may be the result of diverse forms of injury and there is an association between pulmonary diseases and cardiovascular events. The purpose of this study was to evaluate the effects of an angiotensin II type 1 receptor blocker, valsartan, on systemic, cellular, and fibrotic consequences of pulmonary injury induced by the anti-neoplastic antibiotic, bleomycin.

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Left ventricular hypertrophy (LVH) represents an independent risk factor for cardiovascular morbidity and mortality, and normalization of left ventricular mass has become a desirable goal of antihypertensive treatment. In a Suprax Oral Suspension Cost randomized, double-blind study the angiotensin II (AT(1) receptor) antagonist valsartan (Diovan((R)); 80 mg/160 mg q.d.) was compared with the beta-blocker atenolol (50 mg/100 mg q.d.) over 8 months in predominantly previously untreated patients with essential hypertension and LVH. Sixty-nine patients were randomized, of whom 58 were evaluated with echocardiographic data. After 8 months of treatment in the atenolol group [n = 8 with additional hydrochlorothiazide (HCTZ)], initial blood pressure was reduced from 160/103 to 147/92 mm Hg (p < 0.0001), and in the valsartan group (n = 9 with additional HCTZ) blood pressure decreased from 163/101 to 146/90 mm Hg (p < 0.0001). Left ventricular mass index decreased from 127 to 117 g/m(2) in the atenolol group and from 127 to 106 g/m(2) in the valsartan group. Long-term treatment with valsartan resulted in a significant reduction of LVH in patients with essential hypertension.

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This was a prospective, Buy Cleocin Online randomised, 8-month follow-up study that included patients with significant coronary stenosis who received telmisartan (n=36) or valsartan (n=37).

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Double dose of Lipitor Generic Side Effects valsartan combined with tacrolimus treatment of DN patients can improve clinical symptoms, reducing inflammation, inhibiting or even reversing the interstitial fibrosis, which will improve the curative effect and reduce the recurrence, as to provide a new theoretical basis for the clinical treatment of the disease.

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Statin and angiotensin II type 1 receptor blocker therapy improves endothelial dysfunction using distinct mechanisms. We evaluated simultaneous vascular and metabolic responses to pravastatin and valsartan therapy, alone or in combination, in hypercholesterolemic patients. Forty-eight hypercholesterolemic patients (23 had metabolic syndrome) were given pravastatin 40 mg and placebo, pravastatin 40 mg and valsartan 160 mg, or valsartan 160 mg and placebo daily during each 2-month treatment period in a randomized, single-blind, placebo-controlled, crossover trial with three treatment arms and two washout periods (each 2 months). Brachial artery flow-mediated dilation and C-reactive protein improved to a greater extent with combined therapy compared with either monotherapy. Importantly, we also observed simultaneous improvement in metabolic phenotypes, with all three treatments causing increased plasma adiponectin levels, reduced fasting insulin levels, and increased insulin sensitivity relative to baseline measurements. For the first time in a statin combination trial, pravastatin combined with valsartan therapy increased plasma adiponectin, lowered fasting insulin levels, and improved insulin sensitivity in an additive manner when compared with monotherapy alone. In contrast to other statins, hydrophilic pavastatin may be combined with other drugs to safely reach lipid target levels while simultaneously improving the metabolic and Levaquin Generic Picture cardiovascular phenotype of patients at high risk.

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Eight thousand three hundred ninety-nine patients with New York Heart Association class II to IV HF with reduced EF [left ventricular EF (LVEF) ≤40%] were randomized to sacubitril/valsartan 97/103 mg twice daily versus enalapril 10 mg twice daily and followed for a median of 27 months. The primary study end point was cardiovascular death or HF hospitalization. LVEF was assessed at the sites and recorded on case report forms. We related LVEF to study outcomes and assessed the effectiveness of sacubitril/valsartan across the LVEF spectrum. The mean LVEF in PARADIGM-HF, reported by sites, was 29.5 (interquartile range, 25-34). The risk of all outcomes increased with decreasing LVEF. Each 5-point reduction in LVEF was associated with a 9% increased risk of cardiovascular death or HF hospitalization (hazard ratio, 1.09; 95% confidence interval, 1.05-1.13; P<0.001), a 9% increased risk for CV death (hazard ratio, 1.09; 95% confidence interval, 1.04-1.14), a 9% increased risk in HF hospitalization (hazard ratio, 1.09; 95% confidence interval, 1.04-1.14) and a 7% increased risk in all-cause mortality (hazard ratio, 1.07; 95% confidence interval, 1.03-1.12) in adjusted analyses. Sacubitril/valsartan was effective across the LVEF spectrum, with no evidence of heterogeneity, when modeled either in tertiles (P Buy Amoxil Online Uk interaction=0.87) or continuously (P interaction=0.95).

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A woman who for over 15 years of hypertension and its treatment faced difficulties in all domains of sexual function is hereby reported. On reporting this, the beta blocker in her regimen was Olmesartan Benicar Generic replaced by an angiotensin receptor blocker (ARB).

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The continued poor rates of blood pressure (BP) control to the recommended target BP of <140/90 mm Hg in patients Inderal Xl Generic with hypertension indicate a persistent need for improved antihypertensive therapy. Angiotensin II receptor blockers (ARBs) constitute the newest approved class of antihypertensive agents. As with angiotensin converting enzyme inhibitors, ARBs block the renin-angiotensin-aldosterone system, but do so through a more specific mechanism. Angiotensin converting enzyme inhibitors block the conversion of angiotensin I to angiotensin II, but angiotensin II may be produced by several alternate pathways. Angiotensin II receptor blockers, by contrast, inhibit the binding of angiotensin II to the angiotensin II type 1 (AT1) receptor, independent of the pathway of angiotensin II production. Comparative safety and efficacy trials indicate that ARBs are similar to other antihypertensive drugs in terms of BP-lowering effectiveness and have superior tolerability. Olmesartan medoxomil is the newest and one of the most effective of the ARBs. In controlled trials, it has been shown to provide 24-h BP control with antihypertensive efficacy at least as good as that of the calcium channel blockers amlodipine besylate and felodipine and the beta-blocker atenolol. In a comparative study, olmesartan medoxomil demonstrated significantly greater reductions in diastolic BP than did three other leading ARBs-losartan potassium, irbesartan, and valsartan. With the convenience of placebo-like tolerability and once-daily dosing, combined with excellent antihypertensive efficacy, olmesartan medoxomil may be a useful addition to our management of hypertension.

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We analysed data from 5010 patients with stable chronic heart failure and left ventricular dysfunction who were participants in the Val-HeFT study. Individual S&S were stratified by severity. Treatment differences between valsartan and placebo were analysed by S&S strata at baseline and endpoint by logistical regression, and an overall S&S score by ANCOVA. Hazard ratios of S&S strata were calculated for mortality and heart failure hospitalisation. Prognostic contributions of S&S to other variables were determined by multivariate analysis.

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This was a prospective, multinational, non-interventional real-world study in which adult patients with hypertension receiving treatment with Aml/Val or Aml/Val/HCT as part of routine clinical practice were observed for a period of 26 ± 8 weeks. Dosages in milligrams (prescribed in accordance with local prescribing information) were Aml/Val: 5/80, 5/160, 10/160, 5/320 or 10/320; Aml/Val/HCT: 5/160/12.5, 10/160/12.5, 5/160/25, 10/160/25 or 10/320/25.