Increase in bicycloprostaglandin E2 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 E2 metabolite (PGEm), a chemically stable degradation product of the vasodilating prostaglandin E2, were found in response to captopril (39.4 +/- 7.8 vs. 46.2 +/- 8.2 pg/ml; p less than 0.01). With chronic captopril treatment bicyclo-PGEm remained elevated for 12 h after the last dose after 1 and 2 months (75.5 +/- 5.5; p less than 0.05 and 72.1 +/- 6.3 pg/ml; p less than 0.05, respectively). Upon readministration of captopril during chronic captopril treatment the significant increase of bicyclo-PGEm 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 E2 production might play a part in captopril's beneficial action in chronic congestive heart failure.
Stanek
B
B
2nd Department of Internal Medicine, University Hospital, Vienna, Austria.
Punzengruber
C
C
Silberbauer
K
K
D000328:Adult; D000368:Aged; D002216:Captopril / Q000494:pharmacology / Q000627:therapeutic use*; D015232:Dinoprostone / Q000031:analogs & derivatives* / Q000097:blood; D006333:Heart Failure / Q000097:blood* / Q000188:drug therapy; D006801:Humans; D008297:Male; D008875:Middle Aged
C025088:11-deoxy-15-keto-13,14-dihydro-11 beta,16-cycloprostaglandin E2; D002216:Captopril; D015232:Dinoprostone