The involvement of angiotensin II (ANG II) in the genetic polydipsia of the STR/N strain of mice was investigated. Daily water intake of the polydipsic inbred STR/N of both sexes ranged between five and eight times that of nonpolydipsic controls: STR/1N, a mutant of the STR/N, and Swiss-Webster (S/W) mice. Nevertheless the diurnal pattern of drinking was maintained in the STR/N. There was no difference in daily food intake, arterial blood pressure, and plasma renin activity among the three groups. Drinking responses to 48 h of water deprivation were not significantly different between the polydipsic mice and their control groups. Captopril, an angiotensin I converting-enzyme inhibitor, injected subcutaneously just before the dark period, reduced drinking for 6 h in the polydipsic strain only. Food intake of all three groups of mice was not affected. Similarly the ANG II antagonist saralasin, [Sar1,-Ile8]ANG II, injected into the lateral cerebroventricle just before the dark period, significantly reduced water intake for 6 h after injection in the polydipsic mice only. Intracerebroventricular injection of ANG II increased drinking in the nondeprived controls but not in the polydipsic mice. These findings suggest that the polydipsia in the STR/N mice may involve, at least in part, the ANG II system in the brain.
|Journal||American Journal of Physiology - Regulatory Integrative and Comparative Physiology|
|Issue number||6 29-6|
|Publication status||Published - Jan 1 1991|
All Science Journal Classification (ASJC) codes
- Physiology (medical)