Renal Vasodilation by Converting Enzyme Inhibition Role of Renal Prostaglandins

SUMMARY The present study was designed to determine whether renal prostaglandins are in-volved in the renal vasodilation evoked by angiotensin II inhibition in sodium depletion. The convert-ing enzyme inhibitor (CEI) captopril was administered to sodium-depleted control dogs and sodium-depleted 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