Renal Responses to Acetylcholine.

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Abstract
Summary Infusion of Ach into one renal artery of the dog induced unilateral increase in calcium and phosphate excretion and increased GFR, ERPF and excretion of sodium, potassium, chloride and water. Products of Ach hydrolysis, choline and acetate, were inactive. Atropine blocked the renal responses to Ach but exerted no renal actions in the absence of exogenous Ach. Several anticholinesterases failed to alter renal hemodynamic or excretory functions. The excretory changes produced by Ach were not explicable on the basis of changes in GFR alone and indicate that Ach exerted a direct renal tubular action. The data constitute further evidence that cholinergic mechanisms may be regulators of cellular cation transport systems.

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