Key result
Captopril lowers mean blood pressure, an effect blunted by indomethacin and linked to prostaglandin excretion.
Why the study?
The role of endogenous angiotensin II and prostaglandins in the antihypertensive effect of ACE inhibitor captopril in essential hypertension was unclear.
May support prostaglandin contribution to captopril efficacy; leaves open clinical relevance pending larger randomized studies.
The role of endogenous angiotensin II and prostaglandins (PGs) in the antihypertensive effect of converting enzyme inhibitor, captopril, was studied in essential hypertension by the separate and the combined administration of captopril and indomethacin. Although plasma angiotensin II was similarly suppressed by the separate and the combined administration of captopril and indomethacin, captopril lowered and indomethacin increased the mean blood pressure. There were negative correlations between the changes in mean blood pressure and in urinary sodium excretion as well as in urinary PGE excretion. These results suggest that endogenous PGs may be implicated in the antihypertensive effect of captopril through the alteration of sodium balance.
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Omata et al. (1987) studied Essential hypertension. Captopril vs. Indomethacin and combined captopril/indomethacin was evaluated on Change in mean blood pressure. Captopril lowered and indomethacin increased mean blood pressure, with changes negatively correlated with urinary sodium and PGE excretion, suggesting PGs mediate captopril's antihypertensive effect.
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