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Am J Physiol Heart Circ Physiol 261: H714-H719, 1991;
0363-6135/91 $5.00
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AJP - Heart and Circulatory Physiology, Vol 261, Issue 3 714-H719, Copyright © 1991 by American Physiological Society

ARTICLES

Cytochrome P-450-dependent vasodilation of rat kidney by arachidonic acid

A. O. Oyekan, J. C. McGiff and J. Quilley
Department of Pharmacology, New York Medical College, Valhalla 10595.

Our previous studies indicated a role for cytochrome P-450-dependent enzymes in generating the mediators of the vasodilator effect of arachidonic acid (AA) in the preconstricted indomethacin-treated perfused kidney of the rat. We report that in vivo induction of cytochrome P-450 enzymes with 3-methylcholanthrene-beta-naphthoflavone or dexamethasone enhanced the renal vasodilator effect of AA in this experimental preparation. Conversely, depletion of cytochrome P-450 enzymes with stannous chloride or cobalt chloride diminished the vasodilator response to AA. Injection of AA resulted in the release of relaxant material into the renal effluent detected by superfusion of rabbit aortic rings. Inhibition of cytochrome P-450 with 7-ethoxyresorufin reduced the release of vasorelaxant material. Metabolism of labeled AA by the kidney revealed four peaks of radioactivity that were recovered from the renal effluent. The heights of these peaks were reduced by 7-ethoxyresorufin. These results provide further evidence for cytochrome P-450-dependent metabolism of AA to one or more vasodilator products by the rat kidney.


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