Centrally Mediated Hydration Effects of Angiotensin in Various States of Sodium Balance

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Abstract
Angiotensin, present in the central nervous system and kidneys, affects salt/water balance when administered to either site but the relationship between central and peripheral actions is unclear. One reported difference between central and peripheral administration of the peptide is that the former causes natriuresis whereas the latter conserves sodium. We injected angiotensin II into the lateral cerebroventricles of conscious rats maintained on low, normal and high sodium intakes. Prior to injection, plasma [Na+] and hematocrits were similar in the 3 groups. Angiotensin increased plasma vasopressin content in all groups at 1 and 5 min; the 1-min peak was greater in the high Na+ rats. In control and low Na+ rats plasma renin activity (PRA) was suppressed 5 and 20 min after angiotensin. Basal PRA of high Na+ rats was low and tended to be further suppressed by angiotensin. Angiotensin-induced water intake was similar in all groups. Thus, the response pattern to intraventricular angiotensin (vasopressin release, PRA suppression and drinking behavior) occurred over a range of sodium intakes sufficient to suppress or elevate basal PRA. These responses, and the natriuretic effect of intraventricular angiotensin, would be beneficial under conditions of Na+ excess. Conversely, these effects would be detrimental in Na+-defícient conditions since they reduce the ability to maintain extracellular [Na+]. Angiotensin effects in brain may be increased by sodium excess whereas the renal angiotensin system is utilized in response to Na+ deficiency.