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Central angiotensin converting enzyme blockade and thirst.
Pharmacology, Biochemistry, and Behavior
|May 1, 1983
Summary
Central brain angiotensin II plays a minor role in water-deprivation thirst. Captopril, an ACE inhibitor, affected thirst responses differently depending on the substance administered.
Area of Science:
- Neuroscience
- Physiology
- Pharmacology
Background:
- Endogenous brain angiotensin II (AII) is implicated in regulating thirst.
- The role of central AII in various thirst states requires further elucidation.
Purpose of the Study:
- To investigate the role of endogenous brain AII in thirst using the angiotensin converting enzyme inhibitor, captopril.
- To determine the impact of captopril on thirst responses to centrally administered angiotensin I (AI) and AII, as well as other dipsogenic stimuli.
Main Methods:
- Rats were administered captopril intracerebroventricularly (ICV) or intraperitoneally (IP).
- Thirst responses were measured following ICV administration of AI, AII, or carbachol.
- Water intake was assessed in water-deprived rats and rats receiving hypertonic saline.
Main Results:
- ICV captopril attenuated the dipsogenic response to central AI but potentiated the response to central AII.
- Captopril did not alter the response to carbachol.
- Central captopril had minimal effect on water intake in water-deprived rats, while IP captopril potentiated it.
- Central captopril did not affect water intake in rats given hypertonic saline.
Conclusions:
- Central angiotensin converting enzyme plays a minor role in thirst induced by water deprivation.
- The effects of captopril on thirst are dependent on the specific dipsogenic stimulus and route of administration.