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Am J Physiol Heart Circ Physiol (July 24, 2003). doi:10.1152/ajpheart.00075.2003
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Submitted on January 27, 2003
Accepted on July 15, 2003

Nitric Oxide/Epoxygenase Interactions and Arachidonate-induced dilation of the renal microvessel of the rat

I. T. Udosen1, H. C. Hercule1, H. Jiang2, and A. O. Oyekan1*

1 Center for Caardiovascular Diseases, Texas Southern University, Houston, TX, USA
2 Department of Pharmacology, New York Medical College, Valhalla, NY, USA

* To whom correspondence should be addressed. E-mail: Oyekan_AO{at}TSU.EDU.

Nitric oxide (NO) is an inhibitor of hemoproteins including cytochrome P450 (CYP) enzymes. This study tested the hypothesis that NO inhibits CYP epoxygenase dependent vascular responses in the kidney. In the rat renal pressurized microvessel, arachidonic acid (AA, 0.03-1 µM) or bradykinin (BKN, 0.1-3 µM) elicited a NO- and prostanoid-independent vasodilation. Miconazole (1.5 µM) or PPOH (30 µM), inhibitors of epoxygenase enzymes, or fixing epoxide levels with 11,12-epoxyeicosatrienoic acid (11,12-EET; 1 and 3 µM) inhibited these responses as did apamin (1 µM), a large conductance Ca2+-activated potassium channel (BKCa) inhibitor, or 18{alpha}-glycyrrhetinic acid (30 µM), an inhibitor of myoeondothelial gap junctional electromechanical coupling. Spermine NONOate (1 and 3 µM) or sodium nitroprusside (0.3 and 3 µM), NO donors, but not 8-BrcGMP (100 µM), the analog of cGMP, the second messenger of NO, blunted the dilation produced by AA or BKN in a reversible manner without affecting that produced by hydralazine. However, hydralazine, a non-NO donor, did not affect the dilator effect of AA or BKN. However, hydralazine, a non-NO donor, did not affect the dilator effect of AA or BKN. Spermine NONOate did not affect the dilation produced by 11,12-EET, NS-1619, a BKCa opener, or cromakalim, a KATP channel opener. AA and BKN stimulated while hydralazine did not affect EET production. On the other hand, spermine NONOate (3 µM) attenuated basal (19±7%, p<0.05) and AA stimulation (1 µM, 29±9%, p<0.05) of renal preglomerular vascular production of all regioisomeric EETs:-5,6-, 8,9-, 11,12-, and 14,15-EET. These results suggest that NO directly and reversibly inhibits epoxygenase-dependent dilation of the rat renal microvessel without affecting the actions of epoxides on potassium channels.




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