Thirst and sodium appetite after colloid treatment in rats with septal lesions

Previous experiments in which angiotensin II (AII) and mineralocorticoids were administered to rats have suggested that these hormones play a natural role in mediating thirst and sodium appetite. This hypothesis was examined by making use of rats with septal lesions, which have an apparent sensitivity to the central effects of AII, and studying their behavioral response to subcutaneous colloid treatment, which produces hypovolemia and thereby stimulates the secretions of renin and aldosterone. The induced thirst and sodium appetite both were markedly enhanced in the brain-damaged animals. However, water intake was not increased when the hypovolemia was moderate, and sodium appetite was augmented only when animals had been sodium deprived, a procedure known to potentiate aldosterone secretion. These findings support previous suggestions that whereas AII normally contributes little to thirst, it may help to mediate sodium appetite in rats when aldosterone is abundant. Finally, the two drives were not elicited uniformly; those animals that drank the most water after colloid treatment consumed the least saline. These findings suggest that whereas septal lesions may sensitize the rat's brain to the sodium-appetite-eliciting effects of AII as well as to its dipsogenic effects, sodium appetite emerges only if the induced thirst is not too pronounced.