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Increase in plasma aldosterone during prolonged captopril treatment
The American Journal of Cardiology
|April 21, 1982
Summary
Captopril initially suppressed plasma aldosterone but it later increased significantly during long-term angiotensin II suppression, despite sustained hypotension. The exact mechanism for this late aldosterone rise requires further investigation.
Area of Science:
- Endocrinology
- Cardiovascular Pharmacology
Background:
- Angiotensin II plays a key role in regulating aldosterone secretion.
- Captopril, an angiotensin-converting enzyme inhibitor, suppresses the renin-angiotensin-aldosterone system.
Purpose of the Study:
- To investigate the long-term effects of angiotensin II suppression with captopril on plasma aldosterone levels.
- To assess the relationship between aldosterone, renin activity, angiotensin II, and blood pressure during captopril therapy.
Main Methods:
- Seven patients were monitored for plasma aldosterone concentration, plasma renin activity, and plasma angiotensin II levels.
- Measurements were taken before and at various time points during long-term captopril administration.
Main Results:
- Plasma aldosterone initially decreased significantly after 1 month of captopril but then increased substantially after 1 year, exceeding pretreatment levels.
- Plasma renin activity remained elevated, and plasma angiotensin II levels were suppressed throughout the study.
- A sustained hypotensive effect was observed in all patients, with initial body weight decrease followed by recovery.
Conclusions:
- Long-term angiotensin II suppression with captopril leads to an initial decrease followed by a significant late increase in plasma aldosterone.
- The mechanism driving this late aldosterone rise under sustained angiotensin II suppression is not yet understood.
- Captopril effectively suppresses angiotensin II and lowers blood pressure long-term, despite paradoxical aldosterone changes.