During hemorrhagic shock, activation of the renin-angiotensin-aldosterone system helps restore blood pressure. Angiotensin II preferentially constricts the efferent arteriole over the afferent arteriole, helping to maintain GFR. This selectivity exists because:
- A Afferent arterioles dilate via A2 receptors which are activated by locally produced angiotensin I
- B Myogenic autoregulation of the afferent arteriole blocks angiotensin II-induced constriction
- C Efferent arterioles express higher density of AT1 receptors and lack prostaglandin-mediated counter-regulation ✓
- D Afferent arterioles express AT2 receptors that mediate vasodilation opposing AT1 effects
Correct answer: C. Efferent arterioles express higher density of AT1 receptors and lack prostaglandin-mediated counter-regulation
Explanation
The efferent arteriole has a higher density of AT1 receptors relative to the afferent arteriole, making it more sensitive to angiotensin II-mediated vasoconstriction. Additionally, afferent arteriolar tone is buffered by prostaglandins (especially PGE2 and PGI2), which oppose vasoconstriction and are generated locally in response to angiotensin II. This is why NSAIDs, by blocking prostaglandin synthesis, blunt the GFR-protective efferent constriction response during states of reduced renal perfusion, precipitating AKI in susceptible patients.
Reference: Guyton & Hall, Textbook of Medical Physiology, 14th ed.
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