Low dose intrarenal infusions of PGE2, PGI2, and 6-keto-PGE1 vasodilate the in vivo rat kidney.

Abstract

The renal vascular effects of prostaglandin E2 (PGE2), 6-keto-PGE1, and PGI2 were investigated in indomethacin-pretreated rats. These prostanoids were infused directly into the left renal artery at rates ranging from 0.01 to 1.0 microgram/min, while renal blood flow and mean arterial blood pressure were constantly monitored. PGE2, 6-keto-PGE1, and PGI2 produced reductions in mean arterial blood pressure with threshold doses of 1.0, 0.3, and 0.03 microgram/min (P less than 0.01), respectively, and maximal vasodepressor responses of 18.9 +/- 4.3, 37.0 +/- 7.8, and 58.7 +/- 8.2 mm Hg (P less than 0.01), respectively. In addition, all three prostanoids caused a dose-related reduction in renal vascular resistance with a threshold dose of 0.01 microgram/min (P less than 0.05). The maximal reductions in renal vascular resistance were 2.59 +/- 0.52, 4.41 +/- 1.20, and 5.29 +/- 1.06 mm Hg/(ml per min) for PGE2, 6-keto-PGE1, and PGI2 (P less than 0.01), respectively. Whereas PGE2 an 6-keto-PGE1 produced dose-dependent increases in renal blood flow (maximal increases of 1.5 +/- 0.3 and 1.0 +/- 0.3 ml/min, respectively (P less than 0.01), PGI2 nonsignificantly increased renal blood flow at low doses and decreased renal blood flow at higher infusion rates (P less than 0.01). These data indicate that the in vivo rat kidney, similar to the kidneys of other species, is vasodilated by low doses of PGE2, PGI2, and 6-keto-PGE1.