Effects of prostaglandins on vasoconstrictor action in isolated renal arterioles.

The effects of arachidonic acid, prostaglandins (PG) I2, E2, D2, and F2 alpha on norepinephrine- (NE) and angiotensin II- (ANG II) induced tone were examined in interlobular arteries and afferent and efferent arterioles isolated from rabbit kidney. Arachidonic acid at 10(-5) M produced a rapid relaxation of NE-induced tone in all three vessel types. The vasodilatory effect of arachidonic acid but not acetylcholine was blocked by meclofenamate. In interlobular arteries, PGE2, and PGI2 caused a dose-dependent relaxation of NE-induced tone with a concentration causing the half-maximal response (ED50) of 1.2 and 4.6 X 10(-8) M, respectively. PGD2 caused a small but significant relaxation at 10(-7) M and above, whereas PGF2 alpha was inactive. In afferent arterioles contracted with NE, PGE2 and PGI2 caused identical dose-dependent relaxations. Significant effects were observed at concentrations between 10(-11) and 10(-10) M with ED50 values of 1.7 X 10(-8) M for PGE2 and 8.7 X 10(-9) M for PGI2. PGD2 had significant effects only at 10(-5) M, whereas PGF2 alpha was without effect. In contrast to the preglomerular vessels, efferent arterioles responded only to PGI2 (ED50, 9.7 X 10(-9) M), and the other arachidonic acid metabolites had no effect on lumen diameter. PGI2 antagonized the vasoconstrictive effects of both NE and ANG II in this vessel segment. The results demonstrate that of the prostanoids tested only PGE2 and PGI2 were effective in antagonizing vasoconstrictor stimuli in isolated renal microvessels. Furthermore, the rabbit renal microvasculature displays segmental heterogeneity for the vasodilatory PGs in that PGI2 affected both pre- and postglomerular arterioles, whereas PGE2 was effective only on the preglomerular microvessels.