Sympathetic stimulation of the kidney increases renin release via β1-adrenoceptors on juxtaglomerular cells AND causes direct renal vasoconstriction via α1-adrenoceptors. In a hemorrhagic shock patient on high-dose norepinephrine infusion, which of the following is the MOST likely renal consequence?

• A Increased GFR due to enhanced renin-angiotensin mediated efferent arteriolar constriction
• B Reduced renal cortical blood flow leading to ischemic AKI, as NE-mediated afferent and efferent arteriolar vasoconstriction markedly decreases glomerular perfusion ✓
• C Preserved GFR due to autoregulatory dilation of afferent arterioles overcoming NE-mediated constriction
• D Increased urine output due to inhibition of ADH secretion by high sympathetic tone

Explanation

Norepinephrine at high doses (as used in vasopressor therapy) causes potent alpha-1 mediated vasoconstriction of both afferent and efferent renal arterioles. While efferent constriction alone would increase filtration fraction, the dominant effect of high NE is a marked reduction in renal cortical blood flow and GFR, risking ischemic acute kidney injury (ATN). Renal autoregulation (myogenic and tubuloglomerular feedback) is operative at MAPs of 70–160 mmHg; at very low perfusion pressures in shock, autoregulation is overwhelmed. ADH is actually increased by sympathetic activation (baroreceptor-mediated) and hypovolemia, causing water retention — not inhibited.

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

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