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

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Abstract
Renal prostaglandins [PG] may be involved in the renal vasodilation evoked by angiotensin II inhibition in Na+ depletion. The converting enzyme inhibitor (CEI) captopril was administered to Na+-depleted control dogs and Na+-depleted dogs that had previously received the inhibitors of PG 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 PGE2 concentration also increased from 52 to 85 pg/ml (P < 0.01). In the dogs that received inhibitors of PG 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 PGE2 (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 PG synthesis inhibition. In the control dogs RBF after captopril was significantly higher than during the control period; this was not the case in the dogs with PG synthesis inhibition. RBF after captopril and PG inhibition was not significantly different from RBF during the control period. Apparently the acute renal vasodilator effect of captopril in Na+ depletion does not require renal PG, but the level of RBF after captopril is dependent upon renal PG, suggesting that endogenous PG increase renal blood flow when angiotensin II is inhibited. Evidently captopril increases renal PGE2 synthesis.