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The renin-angiotensin system and sodium appetite
Journal De Physiologie
|January 1, 1984
Summary
Intracranial renin and angiotensin II stimulate sodium appetite and thirst. Angiotensin contributes significantly to sodium appetite, especially during hypovolaemia, acting with other factors.
Area of Science:
- Neuroendocrinology
- Physiology
Background:
- Intracranial renin and angiotensin II are known stimuli for sodium appetite and thirst.
- These effects are mediated by local angiotensin II generation, leading to persistent intakes and fluid retention.
Purpose of the Study:
- To investigate the role of renin and angiotensin II in stimulating sodium appetite and thirst.
- To explore the contribution of angiotensin to sodium appetite in conditions of hypovolaemia.
Main Methods:
- Studies involved captopril treatment in adrenalectomized rats.
- Renal hypertension was induced via partial inter-renal aortic ligation in rats.
- Sodium chloride and water intakes were measured.
Main Results:
- Increased circulating renin, induced by captopril or aortic ligation, led to increased intake of 2.7% NaCl and water.
- Fluid intake after aortic ligation was independent of hypertension severity.
- Angiotensin significantly contributed to both sodium appetite and thirst in hypovolaemia.
Conclusions:
- Angiotensin is a key factor in stimulating sodium appetite during hypovolaemia.
- Multiple factors interact to regulate sodium appetite in hypovolaemic states.
- The findings support angiotensin's role in both thirst and sodium appetite regulation.