The contribution of PGI2 to the effects of captopril in conscious dogs in differing states of sodium balance.
There is some evidence that increased prostaglandin synthesis may mediate some of the effects of the angiotensin converting enzyme inhibitor captopril. The potential role of prostaglandin (PG)I2 in this process was assessed by measurement of changes in urinary 6-keto-PGF1 alpha excretion after captopril in eight sodium replete and depleted conscious dogs. In sodium replete animals captopril induced a small decrease in blood pressure, transient increases in effective renal plasma flow and urinary 6-keto-PGF1 alpha excretion, and progressive increases in plasma renin activity (PRA) and urinary sodium excretion. By contrast, during sodium depletion captopril induced a large decrease in blood pressure, a transient increase in effective renal plasma flow and urinary 6-keto-PGF1 alpha excretion, an early large but transient increase in PRA and small progressive increase in sodium excretion. The time course of changes after captopril suggested that increased PGI2 synthesis may contribute to the transient decrease in renal vascular resistance. The increase in PRA during sodium depletion was not associated with any change in urinary 6-keto-PGF1 alpha excretion.
D015121:6-Ketoprostaglandin F1 alpha / Q000652:urine; D000818:Animals; D002216:Captopril / Q000494:pharmacology*; D004285:Dogs; D011464:Epoprostenol / Q000494:pharmacology*; D006439:Hemodynamics / Q000187:drug effects; D008297:Male; D011188:Potassium / Q000652:urine; D012083:Renin / Q000097:blood; D012964:Sodium / Q000494:pharmacology* / Q000652:urine; D014563:Urodynamics / Q000187:drug effects
D015121:6-Ketoprostaglandin F1 alpha; D002216:Captopril; D012964:Sodium; D011464:Epoprostenol; D012083:Renin; D011188:Potassium