Increased Dipsogenic Responsiveness to Angiotensin II in Rats Exposed to Cold: Rate of Loss After Return to Thermoneutral Ambient Temperature

Abstract

Abstract

Subcutaneous administration of angiotensin II (Ang II) to rats exposed chronically to 5°C induced an increased drinking response compared with that of warm-acclimated controls. The exaggerated drinking response was also observed when graded doses of Ang II were administered into the lateral cerebroventricle (icv) of chronically cold-exposed rats. A maximal drinking response occurred in cold-treated, but not in control, rats when the lowest dose of Ang II (1.6 ng/rat) was administered icv. Thus, it is clear that the dipsogenic responsiveness to either centrally or peripherally administered Ang II is increased by chronic exposure to cold. To assess whether the increased responsiveness was retained after removal from cold, graded doses of Ang II were administered to rats removed from cold to a thermoneutral environment. The results again showed a maximal responsiveness to the lowest dose of Ang II administered (25 μg/kg, sc) to cold-treated rats that had either just been removed from cold or removed from cold 2 hr prior to treatment. Cold-exposed rats had an ED₅₀ for Ang II-induced drinking that was about half that of their warm-acclimated controls. To assess how long the cold-induced increase in dipsogenic responsiveness to Ang II lasted after return to a thermoneutral temperature, rats were removed from cold for 24, 48, or 60 hr and then administered graded doses of Ang II (25, 50, or 100 μg/kg, sc). The results suggest that between 46 and 52 hr after removal from cold, the cold-induced increase in dipsogenic responsiveness to Ang II returned to the level of the controls. Hence, the physiological changes in the dipsogenic mechanism induced by exposure to cold are not immediately reversible when the rats are returned to a thermoneutral ambient temperature.