An evaluation of the contribution of cholinergic mechanism to thirst

Evidence is presented which strongly suggests that cholinergic mechanisms are not the exclusive mediators of thirst. Atropine sulfate, delivered systemically, in doses known to eliminate carbachol-induced drinking, did not affect or only partially suppressed drinking induced by: (1) water deprivation; (2) systemic or intracranial cellular dehydration; (3) isosmotic intravascular depletion; (4) systemic injections of renin; or, (5) intracranial injections of angiotensin. It had no effect on the prandial drinking of desalivate rats. Furthermore, bilateral intracranial injections of atropine sulfate in the lateral preoptic or lateral hypothalamic areas exerted only a mild inhibition on the drinking caused by systemic injections of renin, and none at all on drinking following systemic cellular dehydration. The partial contribution of cholinergic mechanisms to thirst makes plausible the findings that drinking caused by cholinergic stimulation differs from that following water deprivation.