Renovascular Hypertension

Renovascular hypertension results from renal artery stenosis (RAS) causing reduced renal perfusion pressure. The juxtaglomerular apparatus senses decreased afferent arteriolar pressure and releases renin, converting angiotensinogen to angiotensin I, which ACE converts to angiotensin II. Angiotensin II causes systemic vasoconstriction, stimulates aldosterone release (promoting sodium/water retention), and activates sympathetic nervous system — all elevating BP. In unilateral RAS, the contralateral kidney experiences hypertension-induced natriuresis ('pressure natriuresis'), partially compensating. In bilateral RAS, both kidneys retain sodium and water without compensation, causing volume-dependent hypertension with flash pulmonary edema. Atherosclerotic RAS (90% of cases) involves ostial plaque extension from the aorta, while FMD (10%) affects mid-to-distal segments.