In a patient with a renal artery stenosis-induced (Goldblatt) hypertension, which sequence of physiological events CORRECTLY describes the pathophysiology?
- A Reduced renal perfusion → decreased renin → reduced angiotensin II → vasoconstriction → hypertension
- B Reduced perfusion of stenosed kidney → increased renin → angiotensin II → aldosterone → sodium retention + vasoconstriction → hypertension ✓
- C Reduced renal perfusion → ADH release → fluid retention → increased cardiac output → hypertension
- D Renal ischemia → prostaglandin E2 release → systemic vasoconstriction → hypertension
Explanation
Renal artery stenosis reduces perfusion pressure to the juxtaglomerular cells, stimulating renin release (beta-1-adrenergic and baroreceptor mechanisms). Renin cleaves angiotensinogen to angiotensin I → ACE converts to angiotensin II. Ang II causes: (1) direct systemic arteriolar vasoconstriction increasing TPR, (2) aldosterone secretion promoting Na+ and water retention expanding ECF volume, and (3) ADH release. Both mechanisms raise MAP — renovascular hypertension. Option A has the direction of renin change reversed. Options C and D involve minor secondary mechanisms.
Reference: Guyton & Hall, Textbook of Medical Physiology, 14th ed.
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