Increase in bicycloprostaglandin E 2 metabolite in congestive heart failure in response to captopril

Vasodilating prostaglandins may be increased in patients with chronic congestive heart failure (CHF) to balance out the effects of vasoconstricting forces. Significant increases in plasma levels of bicycloprostaglandin E 2 metabolite (PGE m ), a chemically stable degradation product of the vasodilating prostaglandin E 2 , were found in response to captopril (39.4±7.8 vs. 46.2±8.2 pg/ml; p<0.01). With chronic captopril treatment bicyclo‐PGE m remained elevated for 12 h after the last dose after 1 and 2 months (75.5±5.5; p<0.05 and 72.1±6.3 pg/ml; p < 0.05, respectively). Upon readministration of captopril during chronic captopril treatment the significant increase of bicyclo‐PGE m in response to captopril was sustained, as were changes in plasma renin activity, angiotensin II, and blood pressure. Plasma catecholamines were unchanged with captopril or decreased slightly, vasopressin remained moderately increased throughout. Taken together, the results suggest that vasodilating prostaglandin E 2 production might play a part in captopril's beneficial action in chronic congestive heart failure.