Valsartan Diovan


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Valsartan is an angiotensin-receptor blocker (ARB) that may be used to manage hypertension and heart failure. Many studies have demonstrated the efficacy of valsartan in reducing blood pressure (BP) in many patient populations (including elderly, women, children, obese patients, patients with diabetes mellitus, patients with chronic kidney disease (CKD), patients at high risk of cardiovascular (CV) disease, African Americans, Hispanic Americans and Asians) and in improving the clinical outcome in cardiovascular (CV) disease and chronic kidney disease (CKD)

Monotherapy: Valsartan may be used alone for the management of hypertension.
Combination therapy: Valsartan is indicated for the management of hypertension in patients for whom combination therapy is deemed appropriate. It is combined with other anthypertensive agents such as hydrochlorothiazide, amlodipine, nevibolol and sacubitril.
Heart Failure: Valsartan is indicated for the treatment of heart failure (NYHA class II-IV) in patients who are intolerant to angiotensin-converting enzyme inhibitors (ACE inhibitors) for various reasons, including those who experience ACE inhibitor adverse effects. In a clinical study of 5010 patients, hospitalizations due to heart failure were markedly decreased when valsartan was taken regularly over a 2-year span

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Valsartan inhibits the pressor effect of an angiotensin II hormone, decreasing blood pressure. Angiotensin II is formed from angiotensin I during a reaction that is catalyzed by angiotensin-converting enzyme, also known as ACE . Angiotensin II is the main pressor agent of the renin-angiotensin system, causing vasoconstriction, aldosterone synthesis and release, cardiac stimulation, as well as the renal reabsorption of sodium.

The cardioprotective benefits of valsartan have been shown in large-scale clinical outcomes trials and include significant decreases in cardiovascular morbidity and mortality in heart failure, after myocardial infarction, and in patients with comorbid hypertension and coronary artery disease and/or heart failure; reductions in heart failure hospitalizations; and reductions in stroke incidence.

This drug has been shown to slow the progression of diabetic nephropathy due to its renoprotective effects. Improvements in chronic kidney disease with valsartan include both clinically and statistically significant decreases in urinary albumin and protein excretion in patients diagnosed with type 2 diabetes and in nondiabetic patients diagnosed with chronic kidney disease.

Mechanism of action

Valsartan selectively acts on AT1, the subtype receptor that mediates the cardiovascular actions of angiotensin II, the main vasoactive hormone of the renin-angiotensin-system. The AT2 receptor subtype, which can be found in tissues such as the brain, endometrium, myometrium, and fetal kidney and adrenals, plays no known role in cardiovascular homeostasis at this time.

Angiotensin II contributes to vasoconstrictor activity and sodium/water retention, which contribute to hypertension. Through the inhibition of response to angiotensin II by actions on the AT1 receptor, valsartan is able to decrease blood pressure.

The cardioprotective effects of valsartan are thought to occur through inverse agonist activity of valsartan on the AT1 receptor, which plays an important role in cardiac remodeling (causing ventricular hypertrophy). Inverse agonists such as valsartan inactivate this receptor, preventing cardiovascular remodeling.


Metabolism: This drug undergoes minimal liver metabolism. Valsartan is not biotransformed to a high degree, as only approximately 20% of a single dose is recovered as metabolites. A hydroxyl metabolite has been found in plasma at low concentrations (less than 10% of the valsartan area under the curve). This metabolite is inactive.

Absorption: Absolute bioavailability for valsartan is approximately 25% (ranges between 10%-35%). The bioavailability of the suspension is 1.6 times higher than that of the oral tablet. With the tablet, food decreases the exposure to valsartan by approximately 40% and peak plasma concentration by approximately 50%. After one oral dose, the antihypertensive activity of valsartan begins within approximately 2 hours and peaks within 4-6 hours in most patients.

Route of elimination: Valsartan, when administered as an oral solution, is mostly recovered in the feces (about 83% of dose) and urine (about 13% of dose).

Half life: After intravenous (IV) administration, valsartan demonstrates bi-exponential decay kinetics (t1/2α <1 hour and t1/2β between 5-9 hours).

Side effects

All medicines may cause side effects, but many people have no, or minor, side effects.Some medical conditions may interact with Valsartan.

Tell your doctor or pharmacist if you have any medical conditions.

Common side effects may include: headache, dizziness, tired feeling, flu symptoms, stomach pain, diarrhea, back pain, joint pain or cough.

Pregnancy: When used in pregnancy, drugs that act directly on the renin-angiotensin system (RAAS) can cause injury and death to the developing fetus. When pregnancy is detected, valsartan should be discontinued as soon as possible.

This is not a complete list of all side effects that may occur. If you have questions about side effects, contact your health care provider.


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