Central angiotensin converting enzyme blockade and thirst.

The role of endogenous brain angiotensin II (AII) in various thirst states was examined in the rat using the angiotensin converting enzyme inhibitor, captopril. Intracerebroventricular (ICV) captopril (7 micrograms) significantly attenuated the dipsogenic response to centrally administered angiotensin I (AI) (200 ng) for up to 2 hours. The same dose of captopril significantly potentiated the dipsogenic response to ICV AII (100 ng) but failed to alter the dipsogenic response to ICV carbachol (200 pmoles). Central pretreatment with captopril (7 micrograms), for 30 minutes, failed to alter markedly the cumulative water intake of 24 hour water deprived rats. However, a small, significant 8% decrease in water intake was noted in ICV captopril treated rats 60 minutes following the return of water. The same dose of captopril, administered intraperitoneally, significantly potentiated the cumulative water intake of 24 hour water deprived rats. Central pretreatment with captopril (7 micrograms), for 30 minutes, failed to alter the cumulative water intake of rats treated intraperitoneally with hypertonic saline (0.75 M given at a dose of 1% of the body weight). From these studies it would appear that central angiotensin converting enzyme plays only a minor role in thirst induced by water deprivation.