Renal artery stenosis (RAS) causes renovascular hypertension. In unilateral RAS, the primary sustained mechanism of hypertension after the initial weeks is:

• A Persistent renin hypersecretion from the ischaemic kidney maintaining elevated angiotensin II
• B Sympathetic activation from renal ischaemia raising peripheral resistance
• C Aldosterone-independent mineralocorticoid hypertension from adrenal hyperplasia
• D Sodium and water retention by the contralateral kidney (Goldblatt hypertension — pressure natriuresis shifted rightward) ✓

Explanation

In the Goldblatt (one-clip two-kidney) model of unilateral RAS, initial renin secretion drives angiotensin II and hypertension. Over weeks, the contralateral normal kidney — exposed to the high systemic blood pressure — pressure natriuresis should correct volume; however, angiotensin II directly impairs natriuresis in the contralateral kidney, allowing sodium retention. The sustained mechanism is therefore body fluid volume expansion (sodium and water retention shifting the pressure-natriuresis curve rightward) along with residual angiotensin II effects — not simply persistent renin elevation from the stenotic kidney, which partially normalizes.

Reference: Guyton & Hall, Textbook of Medical Physiology, 14th ed.

High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP

Written and medically reviewed by the StethoPrep medical team.