A 55-year-old man with cirrhosis develops hepatorenal syndrome with creatinine rising to 2.8 mg/dL despite albumin challenge and withdrawal of diuretics. The drug given to improve renal perfusion in this setting works by:

• A Selective dopamine D1 receptor agonism causing renal vasodilation
• B Endothelin ETA receptor antagonism reversing intrarenal vasoconstriction
• C Beta-1 adrenergic stimulation raising cardiac output preferentially to the kidneys
• D Vasopressin V1-mediated splanchnic vasoconstriction improving effective arterial blood volume ✓

Explanation

Terlipressin, a synthetic vasopressin analogue, is the established therapy for hepatorenal syndrome when combined with albumin. It constricts splanchnic capacitance vessels via V1 receptors, correcting the extreme arterial vasodilation of advanced cirrhosis and restoring effective arterial blood volume, which reflexly improves renal perfusion. Low-dose dopamine lacks benefit in trials, beta-1 stimulation does not reverse the splanchnic vasodilatory state, and endothelin antagonists are not standard therapy here.

Reference: Harrison's Principles of Internal Medicine, 21st ed.

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