1. Bilateral nephrectomy or bilateral ureteric ligation greatly reduced the intake and retention of sodium in sodium‐depleted adrenalectomized rats which were experienced at drinking aversive concentrations of saline and which otherwise would have drunk and retained substantial quantities of sodium. 2. Pharmacological activation of the renin—angiotensin system with isoprenaline or phentolamine caused increased intake of water but did not stimulate sodium appetite in sodium‐replete adrenalectomized rats, and decreased sodium appetite in sodium‐depleted adrenalectomized animals. 3. Neither I.P. injections of renin nor intravenous infusions of angiotensin II stimulated sodium appetite in normal rats or sodium‐replete adrenalectomized rats. 4. 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. 5. 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 sodium depleted. 6. Similar preoptic injections in sodium‐depleted adrenalectomized rats caused increased water intake but did not increase the saline intake any further. 7. Intracranial injections of carbachol had little effect on saline intake in either sodium‐replete or sodium‐depleted adrenalectomized rats but caused increased water intake. 8. In conclusion, peripheral activation of the renin—angiotensin system stimulates water intake but has no direct effect on sodium appetite. Secondly, central administration of components of the renin—angiotensin system causes thirst and does not inhibit sodium appetite whereas centrally administered carbachol causes thirst and inhibits sodium appetite. Therefore the renin—angiotensin system has only a minor role in sodium appetite.
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