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 indications

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]
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]
The clinical EXCITE (EXperienCe of Amlodipine and Valsartan in hypErtension) study evaluated the effectiveness and safety of Amlodipine/Valsartan (Aml/Val) and Amlodipine/Valsartan/hydrochlorothiazide (Aml/Val/HCT) single-pill combinations (SPCs) over a period of 26±8 weeks in patients with hypertension in a real-world setting in the Middle East and Asia. [source, 2015]
The over-expression of CK2 in cells treated with Valsartan abrogated its beneficial effect on KCNJ2/Kir2.1 (Fig. 4c). [source, 2015]
Additionally, as the EMSA results indicate, Valsartan eliminated the phosphorylation effect of CK2 on Sp1, resulting in a higher KCNJ2 expression level than in the CK2 group (Fig. 4d). [source, 2015]
To identify whether TBB and Valsartan have an effect on Kir2.1 expression through the endogenous CK2, we introduced TBB and Valsartan on H9c2 rat ventricular cells without CK2 intervention. [source, 2015]
Both TBB and Valsartan have insignificant inhibitory effects on the endogenous CK2 as well as Kir2.1 expression (Fig. 5). [source, 2015]
Additionally, our findings indicate that CK2 is a potential mediator of the electrophysiological effects of Valsartan and provide a basis for the improvement of IK1 remolding facilitated by Valsartan. [source, 2015]
This effect was repressed by the highly selective cell permeable CK2 inhibitor, TBB, and Valsartan. [source, 2015]
Valsartan presents a similar effect on CK2 regulation. [source, 2015]