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Increase in prostaglandins during converting enzyme inhibition
Clinical Science (London, England : 1979)
|December 1, 1980
Summary
Captopril, an angiotensin-converting enzyme inhibitor, increases vasodilatory prostaglandin E2 levels, contributing to its blood pressure-lowering effects. This mechanism is independent of sodium intake levels in healthy individuals.
Area of Science:
- Cardiovascular Pharmacology
- Renal Physiology
Background:
- Angiotensin II and bradykinin changes do not fully explain captopril's hypotensive effect.
- Prostaglandins are implicated in blood pressure regulation.
Purpose of the Study:
- To investigate the role of plasma prostaglandins in the hypotensive response to captopril.
- To assess the influence of sodium intake on this relationship.
Main Methods:
- Nine healthy males received increasing doses of captopril.
- Plasma prostaglandin metabolites were measured under high and low sodium diets.
- Blood pressure changes were correlated with prostaglandin levels.
Main Results:
- Captopril significantly increased 13,14-dihydro-15-keto prostaglandin E2 metabolite on both high and low sodium diets.
- This increase in prostaglandin E2 metabolite strongly correlated with the reduction in blood pressure.
- No significant changes were observed in 6-keto-prostaglandins F1 alpha or thromboxane B2.
Conclusions:
- Increased prostaglandin E2 metabolite is a significant factor in captopril-induced hypotension.
- The effect of captopril on prostaglandin E2 is not significantly influenced by dietary sodium levels.
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