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Peripheral angiotensin causes salt appetite in rats
1Department of Psychology, University of Iowa, Iowa City 52242.
The American Journal of Physiology
|July 1, 1994
Summary
Sodium depletion triggers salt appetite, but this study shows renal angiotensin (ANG) is crucial. Cerebral ANG is not the sole cause, challenging existing theories on salt appetite regulation.
Area of Science:
- Physiology
- Neuroscience
- Endocrinology
Background:
- The established theory posits that central angiotensin (ANG) drives salt appetite following sodium depletion.
- This theory relies on experiments using angiotensin-converting enzyme (ACE) inhibitors, like captopril, to block ANG production.
Purpose of the Study:
- To re-evaluate the role of central versus renal angiotensin in sodium depletion-induced salt appetite.
- To investigate the efficacy of captopril in blocking both central and peripheral ACE in vivo.
Main Methods:
- Rats with sodium depletion-induced salt appetite were infused with captopril (2.5 mg/h).
- Water intake responses to central ANG I injections were measured.
- Arterial pressure responses to intravenous ANG I, intravenous ANG II, and central ANG I were assessed.
Main Results:
- Captopril infusion blocked peripheral ACE, indicated by the absence of pressor response to intravenous ANG I.
- Central ACE remained functional, as evidenced by normal water intake and pressor responses to central ANG I.
- Peripheral ACE blockade did not abolish salt appetite, suggesting a different mechanism.
Conclusions:
- The study demonstrates that angiotensin (ANG) of renal origin is essential for sodium depletion-induced salt appetite.
- Existing theories attributing salt appetite solely to cerebral ANG are challenged.
- Central ACE is not fully inhibited by the tested captopril dose, indicating incomplete central blockade.