valsartan

Valsartan competitively antagonizes the angiotensin II type 1 (AT1) receptor, blocking vasoconstriction, aldosterone release, sympathetic activation, and ADH secretion that would otherwise be triggered by angiotensin II. Unlike ACE inhibitors, ARBs do not inhibit ACE, so bradykinin levels are not increased—this explains the lower incidence of dry cough and angioedema compared to ACE inhibitors, making valsartan a preferred alternative in patients intolerant to ACEIs. Clinical indications include essential hypertension, heart failure with reduced ejection fraction (as part of guideline-directed medical therapy, including sacubitril/valsartan combination—Entresto), and post-myocardial infarction management to reduce cardiac remodeling. Valsartan is also renoprotective in diabetic nephropathy by reducing intraglomerular pressure via efferent arteriolar dilation, decreasing proteinuria. Key adverse effects include hyperkalemia (due to reduced aldosterone), hypotension, and acute kidney injury—especially in bilateral renal artery stenosis, where GFR is highly dependent on angiotensin II-mediated efferent arteriolar constriction. Valsartan is contraindicated in pregnancy (teratogenic, causes fetal renal damage, oligohydramnios, and skull ossification defects) and should not be combined with ACE inhibitors or direct renin inhibitors due to increased risk of hyperkalemia and renal impairment. It requires dose adjustment in hepatic and renal impairment. High-yield boards association: ARBs and ACEIs both require monitoring of potassium and creatinine after initiation, and both are first-line in diabetic patients with proteinuria for renoprotection independent of blood pressure effects.