Thirst in Brattleboro rats.

Thirst mechanisms in Brattleboro rats are activated because of a deficiency in circulating vasopressin. Plasma osmolality, renin, and angiotensin II (ANG II) are increased. We measured the responsiveness of Brattleboro rats and appropriate control strains to cellular and extracellular thirst stimuli taking the spontaneous base-line water intake into account. Brattleboro rats drank more in response to intraperitoneal hypertonic NaCl than controls, but when their fluid losses were prevented by nephrectomy they did not overdrink. Despite low urinary concentration, Brattleboro rats excreted the sodium load at least as rapidly as the controls. Brattleboro rats drank after intracranial injection of renin, renin substrate, and ANG I and II. The dose-response curves were similar to controls, although the Nottingham Long-Evans control strain drank significantly less in response to some doses of the peptides. Intracranial captopril inhibited renin- and ANG I-induced but not ANG II-induced drinking. Isoproterenol reduced spontaneous drinking of Brattleboro rats but increased drinking in controls. However, when urinary losses were prevented by ureteric ligation, isoproterenol caused markedly greater water intake in Brattleboro rats than in controls. Subcutaneous captopril in moderate, thirst-enhancing doses also caused a larger increase in water intake in Brattleboro rats than in controls. Therefore the renin-angiotensin system of Brattleboro rats is more responsive to renin-dependent thirst challenges than that of normal controls.