Latest research on Valsartan

Valsartan is an angiotensin-receptor blocker (ARB) that may be used to treat a variety of cardiac conditions including hypertension, diabetic nephropathy and heart failure. Valsartan lowers blood pressure by antagonizing the renin-angiotensin-aldosterone system (RAAS); it competes with angiotensin II for binding to the type-1 angiotensin II receptor (AT1) subtype and prevents the blood pressure increasing effects of angiotensin II. Unlike angiotensin-converting enzyme (ACE) inhibitors, ARBs do not have the adverse effect of dry cough. Valsartan may be used to treat hypertension, isolated systolic hypertension, left ventricular hypertrophy and diabetic nephropathy. It may also be used as an alternative agent for the treatment of heart failure, systolic dysfunction, myocardial infarction and coronary artery disease.

Valsartan side effects

The recent PARADIGM-HF multicenter randomized controlled trial [116] tested a drug that is a combination of the ARB Valsartan and the neprilysin inhibitor sacubitril on 8399 patients with heart failure and a reduced LVEF, reporting a reduction of 20% in death from cardiovascular causes or hospitalization for heart failure as compared with the ACE inhibitor Enalapril alone at maximum dosage (p < 0.001). [source, 2016]
A centrally administered AT1R-selective antagonist, Valsartan (10 nmol per rat, icv), significantly diminished the Ang II (0.01 and 0.02 nmol per rat, icv)-induced decrease in ICI. [source, 2016]
Pretreatment with a centrally administered AT2R-selective antagonist, PD123319, or peripherally administered Valsartan or PD123319 (intravenous, iv) had no effect on the Ang II-induced decrease in ICI. [source, 2016]
Pretreatment with peripheral administration of Valsartan, an AT1R-selective antagonist, or PD123319, an AT2R-selective antagonist, failed to inhibit the Ang II-induced decrease in ICI. [source, 2016]
Alternatively, central administration of Valsartan, but not PD123319, prevented the Ang II-induced decrease in ICI. [source, 2016]
Our previous reports showed that centrally administered Ang II (3 nmol per rat, icv) elevated SBP and DBP, and that these increases were abolished by Valsartan in the rat7. [source, 2016]
Central administration of 10 nmol Valsartan was performed because the icv-administration of 100 nmol Valsartan caused hypotensive effects in our preliminary study. [source, 2016]
Moreover, centrally administered Valsartan (10 nmol) or PD123319 (100 nmol) was chosen because these drugs failed to affect urodynamic parameters in rats. [source, 2016]
Subeq [27] reported that intravenous administration of 3 mg/kg/day Valsartan ameliorated chlorhexidine digluconate-induced peritoneal fibrosis by decreasing serum and dialysate TGF-β1 levels and significantly decreased the expression of TGF-β1, α-SMA, fibronectin, collagen and VEGF in rats’ peritoneum. [source, 2015]
Therefore, we used a rat model of MI to determine whether the angiotensin type 1 receptor antagonist, Valsartan, downregulates CK2 and increases the expression of Kir2.1 following MI. [source, 2015]