The renin‐angiotensin system and sodium appetite

Abstract

Bilateral nephrectomy or bilateral ureteric ligation greatly reduced the intake and retention of Na in Na-depleted adrenalectomized rats which were experienced at drinking aversive concentrations of saline and which otherwise would have drunk and retained substantial quantities of Na. Pharmacological activation of the renin-angiotensin system with isoprenaline or phentolamine caused increased intake of water but did not stimulate Na appetite in Na-replete adrenalectomized rats, and decreased Na appetite in Na-depleted adrenalectomized animals. Neither i.p. injections of renin nor i.v. infusions of angiotensin II stimulated Na appeptite in normal rats or Na-replete adrenalectomized rats. No differences were found in the saline preference-aversion curves of normal rats not maintained on saline given intracranial injections of angiotensin II or carbachol. Preoptic injections of renin, renin substrate or angiotensin II into sodium-replete adrenalectomized rats which were maintained on water and 2.7% saline induced immediate thirst followed by some saline intake. The saline intake was markedly less than the spontaneous saline intake of the same rats when Na depleted. Similar preoptic injections in Na-depleted adrenalectomized rats caused increased water intake but did not increase the saline intake any further. Intracranial injections of carbachol had little effect on saline intake in either Na-replete or Na-depleted adrenalectomized rats but caused increased water intake. Peripheral activation of the renin-angiotensin system stimulates water intake but has no direct effect on Na appetite. Central administration of components of the renin-angiotensin system causes thirst and does not inhibit Na appetite whereas centrally administered carbachol causes thirst and inhibits Na appetite. The renin-angiotensin system has only a minor role in Na-appetite.