Renal vasodilation by converting enzyme inhibition. Role of renal prostaglandins.

The present study was designed to determine whether renal prostaglandins are involved in the renal vasodilation evoked by angiotensin II inhibition in sodium depletion. The converting enzyme inhibitor (CEI) captopril was administered to sodium-depleted control dogs and sodiumdepleted dogs that had previously received the inhibitors of prostaglandin synthesis, indomethacin or meclofenamate. CEI in control dogs increased renal blood flow (RBF) from a mean value of 220 to 309 ml/min (p < 0.01) and decreased renal vascular resistance (RVR) from 0.64 to 0.38 arbitrary resistance units (ru) (p < 0.01). Renal venous prostaglandin E2 (PGE2) concentration also increased from 52 to 85 pg/ml (p < 0.01). In the dogs that received inhibitors of prostaglandin synthesis, RBF fell from 214 to 168 ml/min (p < 0.01), RVR increased from 0.61 to 0.82 ru (p < 0.05), and renal venous PGE2 fell from 114 to 20 pg/ml.(p < 0.01). The subsequent administration of captopril increased RBF from 168 to 221 ml/min (p < 0.01), lowered RVR from 0.82 to 0.43 ru (p < 0.01), but failed to significantly increase renal venous~RGE2 (20 to 25 pg/ml). The decrease in RVR induced by captopril was not significantly different in the control dogs and in the dogs with prostaglandin synthesis inhibition. However, in the control dogs RBF after captopril was significantly higher than during the control period; this was not the case in the dogs with prostaglandin synthesis inhibition. RBF after captopril and prostaglandin inhibition was not significantly different from RBF during the control period. The results indicate that the acute renal vasodilator effect of captopril in sodium depletion does not require renal prostaglandins; however, the level of RBF after captopril is dependent upon renal prostaglandins, suggesting that endogenous prostaglandins increase renal blood flow when angiotensin II is inhibited. The results confirm previous studies indicating that captopril increases renal PGE2 synthesis. (Hypertension 5: 166-171, 1983)