The effect of prostaglandin synthesis inhibition of the acute blood pressure reduction by captopril in pentobarbital-anaesthetized rats

Abstract

Treatment of pentobarbital-anaesthetized rats with captopril (SQ 14225) caused a reduction in mean arterial blood pressure (MAP), which lasted for over 1 h when a dose of 5 mg/kg i.p. was used. Pretreatment with the prostaglandin synthesis inhibitors indometacin (IND, 5 mg/kg i.p.) or acetylsalicylic acid (ASA, 100 mg/kg i.p.) did not prevent the initial decrease in MAP after captopril. However, the recovery of the MAP was much faster than after captopril alone. In rats pretreated with IND, the MAP after captopril was significantly higher than after captopril alone from 30 min onwards. With ASA pretreatment the same was observed after 45 min. These data indicate that the subacute blood pressure lowering effect of captopril in pentobarbital-anaesthetized normotensive rats may be at least partly dependent on the presence of an intact prostaglandin biosynthetic pathway. This may be due to activation of prostaglandin synthesis by the accumulation of bradykinin and angiotensin I after captopril.