Renin‐induced sodium appetite: effects on sodium balance and mediation by angiotensin

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Abstract
Injection of pig renin or purified renin from the mouse submaxillary gland into the preoptic region or 3rd ventricle of the rat caused thirst within a minute or so of injection followed shortly afterwards by increased Na appetite. Renin from 2 widely different sources produced identical responses. The stimulating effect of renin on intake of water and hypertonic (2.7%) NaCl was continuous and persisted for at least a wk after the largest (265 ng) dose of purified renin. The stimulating effect was also very large. A single preoptic injection of less than 0.75 pmol (26.5 ng) purified mouse renin caused mean intakes of 250.4 .+-. 26.2 ml water and 44.8 .+-. 12.5 ml 2.7% NaCl by 5 naive rats in 24 h. After the largest dose (265 ng) intakes of water and 2.7% NaCl reached .apprx. 80% and 20% body weight, respectively. Weekly injections of renin resulted in progressively larger intakes of NaCl and water in response to the injections. Even after repeated injections, carbachol did not stimulate Na appetite. The stimulating effect on water intake was quickly over and showed no progressive increase with repeated injections. Overnight intake of water was generally depressed after carbachol. Preoptic injection renin caused some increase in Na excretion but this was small compared with the stimulating effect on Na appetite. Detailed temporal analysis of fluid and Na balance shows that the increased intakes of water and 2.7% NaCl were not secondary to renin-induced urinary losses. Increased intakes of water and 2.7% NaCl caused by renin resulted in the rats going into and remaining in positive fluid and Na balance throughout the 24 h experiment. Renin-induced Na appetite and thirst were inhibited by the converting enzyme inhibitors, teprotide or captopril, or by the angiotensin antagonist, saralasin. Inhibition was longer lasting after captopril. Carbachol-induced thirst was unaffected. Renin injected into the preoptic region or 3rd ventricle is a potent stimulus to Na appetite as well as thirst. The effect is mediated by local generation of angiotensin II and it is not secondary to increased urinary loss.