Abstract
Discussion and Conclusions
In order to determine the extent to which the increase in renal blood flow contributed to the natriuretic action of acetylcholine, a variable resistance clamp was placed around the aorta proximal to the renal artery and tightened as necessary to prevent the acetylcholine-induced increase in renal blood flow. Thus, if the natriuresis caused by acetylcholine was due solely to the increased renal blood flow, prevention of this increase with the aortic clamp would result in no increase in sodium excretion. It was demonstrated that sodium excretion after acetylcholine infusion and with renal blood flow held constant, was significantly decreased from control. In the absence of acetylcholine, a decrease in perfusion pressure equal to that needed with acetylcholine to hold renal blood flow constant also resulted in a significant decrease in sodium excretion (Table III). The fact that there were no significant differences between data of the acetylcholine-clamp experiments and the saline-clamp experiments indicates that the natriuretic action of acetylcholine is entirely dependent upon the increase in renal blood flow produced by the agent and does not result from an effect upon active tubular reabsorption of sodium.
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