Differential effects of brain lesions on thirst induced by the administration of angiotensin-II to the preoptic region, subfornical organ and anterior third ventricle.

(1) The possibility that water intake elicited by the administration of angiotensin-II to the preoptic region (POA), subfornical organ and anterior third ventricle is mediated by separate neural systems was investigated in 58 male Wistar rats using electrolytic lesion techniques. (2) Lesions of the midlateral hypothalamus and paramedial rostral midbrain produced a significant reduction in water intake to angiotensin-II microinjected into the POA but did not affect drinking following administration of angiotensin-II to the subfornical organ or anterior third ventricle. (3) Ablation of the midlateral hypothalamus, paramedial rostral midbrain, habenular nucleus or interpeduncular nucleus had no significant effect on water intake elicited in response to microinjection of carbachol or hypertonic saline into the preoptic region, subfornical organ or anterior third ventricle. (4) In a second series of 12 animals lesions of the subfornical organ attenuated water intake in response to a peripheral injection of renin or isoproteronol without disrupting drinking to peripheral administration of hypertonic saline or polyethylene glycol or to 24 h water deprivation. (5) It is concluded that separate neural systems mediate water intake elicited by administration of angiotensin-II to the preoptic area, subfornical organ and anterior third ventricle. The possible physiological significance of independent and parallel peripheral and cerebral renin-angiotensin systems for the control of drinking behavior mediated by angiotensin-II is discussed. (6) The present results are in agreement with previous work which indicates that water intake induced by central administration of angiotensin-II, carbachol and hypertonic saline is subserved by different neural substrates.