Effect of acetylcholine, atropine, and physostigmine on renal function in the dog

¹ Department of Physiology, The University of Michigan, Ann Arbor, Michigan

Acetylcholine (1–500 µg/min), atropine (.002–.12 mg/kg min), or physostigmine (.01–.08 mg/min) was infused directly into the left renal artery of anesthetized dogs, and right and left kidney functions were compared. Acetylcholine produced variable changes in glomerular filtration rate (–30 to +55%), but always increased renal plasma flow (4–115%), sodium excretion (20–365 µm/min), potassium excretion (1–56 µm/min), and urine volume (.25–3.1 ml/min). Filtration fraction, urine osmolality, and medullary sodium concentration were always reduced. These changes could all be reversed or prevented by atropine. Stop-flow studies failed to demonstrate any distal tubular inhibition of sodium reabsorption by acetylcholine. Neither atropine nor physostigmine, when infused into the renal artery by itself, produced any changes in renal hemodynamics or electrolyte excretion. These data demonstrate that acetylcholine can decrease renal arteriolar resistance and inhibit tubular sodium reabsorption. They also provide indirect evidence which supports, but does not prove, the hypothesis that the kidney lacks parasympathetic innervation.

Key Words: cholinesterase inhibitors • renal circulation • renal electrolyte excretion • renal countercurrent system renal innervation

Submitted on June 14, 1963

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