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Increase in cardiovascular reactivity following bilateral nephrectomy has previously been found to be independent of the presence of the central nervous system, mechanical exclusion of the renal vascular bed, or loss of renal excretory function. It was considered possible that increased responsiveness results from removal of endogenous stores of renin. In nephrectomized dogs treated with crude kidney extracts, or infused continuously with synthetic angiotensin for 48 hours, enhancement of response to angiotensin and renin was inhibited while that to norepinephrine was not; response to tyramine was augmented as after infusion of angiotensin into intact dogs. Treatment with liver extracts alone did not inhibit response to renin or angiotensin; neither did continuous infusion of norepinephrine. When hog renin was added to liver extracts, the combination had the same inhibitory effect as kidney extracts. The data are in accord with the concept that depletion of endogenous renin contributes to the enhanced pressor responsiveness that occurs following bilateral nephrectomy.

Increased Cardiovascular Reactivity Caused by Depletion of Endogenous Renin in Dogs