zd-7155 and Dehydration

The contribution of brain angiotensin II (ANG II) to thirst and Na+ appetite of sheep was evaluated. Thirst was stimulated by water deprivation, intracarotid or intracerebroventricular infusion of ANG II, or intracarotid or intracerebroventricular infusion of hypertonic solution. Intracerebroventricular infusion, over 1-3 h, of the ANG II type 1 (AT1) receptor antagonist, losartan, decreased or abolished water intake caused by all of the stimuli tested. Intracerebroventricular infusion of ZD-7155, another AT1-receptor antagonist, blocked ANG II-induced water intake. Neither losartan nor ZD-7155 infused intracerebroventricularly altered the Na+ appetite of Na(+)-depleted sheep. Intracerebroventricular infusion of losartan over 3 h, however, did block the increase in water intake and the decrease in Na+ intake caused by intracerebroventricular infusion of hypertonic NaCl in Na(+)-depleted sheep. Intracerebroventricular infusion of the ANG II type 2 (AT2) receptor antagonist, PD-123319, over 1-3 h, did not alter ANG II-induced water intake or Na+ depletion-induced Na+ intake. These results are consistent with the proposition that brain ANG II, working via AT1 receptors, is involved in the neural system controlling some aspects of physiological thirst and Na+ appetite. A role for AT2 receptors in physiological thirst or Na+ appetite is not supported by the present results.

Topics: Analysis of Variance; Angiotensin II; Angiotensin Receptor Antagonists; Animals; Appetite; Biphenyl Compounds; Brain; Cerebral Ventricles; Dehydration; Diet, Sodium-Restricted; Diuresis; Female; Imidazoles; Infusions, Parenteral; Losartan; Mannitol; Naphthyridines; Pyridines; Receptor, Angiotensin, Type 1; Receptor, Angiotensin, Type 2; Saline Solution, Hypertonic; Saliva; Sheep; Sodium, Dietary; Tetrazoles; Thirst