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In adrenalectomized, deoxycorticosterone-treated and normal rats, injection of angiotensin II through a cannula implanted in the preoptic region caused increased intakes of hypertonic NaCl and water when both fluids were available, whereas injection of carbachol through the same cannula only caused increased water intake. Carbachol depressed NaCl intake of adrenalectomized rats that were allowed access to hypertonic NaCl after being deprived of it for 24 h. Angiotensin-stimulated rats were more likely to go into positive sodium balance than controls, whereas carbachol-stimulated animals were more likely to go into negative balance. After angiotensin, adrenalectomized or deoxycorticosterone-treated rats drank a larger proportion of their total fluid intake as hypertonic NaCl than did normal rats. Angiotensin caused significant increases in sodium excretion in normal, isotonic saline-loaded and deoxycorticosterone-treated rats, but not in adrenalectomized rats, although angiotensin caused increased intakes of NaCl in all groups. On the other hand, carbachol caused a significant increase in sodium excretion at 1 h in all groups despite the absence of an increase in NaCl intake. After angiotensin, only normal rats showed a significant kaliuresis at 1 h, whereas all carbachol-injected rats showed increased potassium excretion. Therefore, angiotensin is a primary stimulus to increased sodium appetite, normally acting in conjunction with other stimuli which enhance its effect, whereas carbachol is a central inhibitor of sodium appetite.

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