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Vol. 292, Issue 3, 1153-1160, March 2000

Cytochrome P450 omega /omega -1 Hydroxylase-Derived Eicosanoids Contribute to EndothelinA and EndothelinB Receptor-Mediated Vasoconstriction to Endothelin-1 in the Rat Preglomerular Arteriole1

Hantz C. Hercule and Adebayo O. Oyekan

Department of Pharmacology, New York Medical College, Valhalla, New York

The preglomerular arteriole of the rat was used to evaluate the contribution of cytochrome P450-derived eicosanoids to the vasoconstrictor effect of endothelin (ET)-1 and to determine the receptors mediating the response. ET-1 (4 × 10-11 to 2 × 10-9 M) produced dose-dependent reductions in the intraluminal diameter of the renal arteriole ranging from 25 ± 8 to 142 ± 16 µm. BMS182874 [(5-dimethylamino)-N-(3,4-dimethyl-5-isoxazolyl)-1-naphthalenesulfonamide; 3 µM], an ETA receptor antagonist, or BQ788 (N-cis-2,6-dimethyl-piperidino-carbonyl-L-gamma -methylleucyl-D-1-methoxycarbonyl-tryptophanyl-D-norleucine; 1 µM), an ETB receptor antagonist, attenuated ET-1 vasoconstriction by 59 ± 4 and 50 ± 10%, respectively. The combined administration of both ET receptor antagonists increased inhibition of ET-1 vasoconstriction to 75 ± 4%. 17-Octadecynoic acid (17-ODYA, 2 µM) or 12,12-dibromododec-enoic acid (2 µM), inhibitors of 20-hydroxyeicosatetraenoic acid (20-HETE) production, attenuated ET-1-induced vasoconstriction by 50 ± 6 and 40 ± 3%, respectively, as did indomethacin (10 µM), an inhibitor of cyclooxygenase. Miconazole (2 µM), the epoxygenase inhibitor, was without effect. 20-HETE (10-8 and 2 × 10-8 M) elicited a dose-related vasoconstriction that was inhibited by 10 µM, but not 5 µM, indomethacin. The inhibition by 17-ODYA of ET-1 vasoconstriction was not greater when combined with BMS182874 or BQ788. Moreover, vasoconstriction induced by ET-3, an ETB-selective agonist, was inhibited by 17-ODYA. These data indicate that both ETA and ETB receptors mediate ET-1 vasoconstriction and that 20-HETE production linked to both receptors makes a major contribution to ET-1-induced renal arteriolar vasoconstriction in the rat.

1 This work was supported by National Institutes of Health Grant RO1-HL25394 and RO1-HL59884. This study was presented at the Experimental Biology '99 Meeting in Washington, DC, April 7-21, 1999.

0022-3565/00/2923-1153$03.00/0
THE JOURNAL OF PHARMACOLOGY AND EXPERIMENTAL THERAPEUTICS
Copyright © 2000 by The American Society for Pharmacology and Experimental Therapeutics


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