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Am J Physiol Heart Circ Physiol 281: H1553-H1560, 2001;
0363-6135/01 $5.00
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Vol. 281, Issue 4, H1553-H1560, October 2001

Endothelium-derived hyperpolarizing factor in coronary microcirculation: responses to arachidonic acid

Christine L. Oltman1, Neal L. Kane1,2, Jonathon L. Fudge2, Neal L. Weintraub2, and Kevin C. Dellsperger1,2

1 Department of Veterans Affairs, Iowa City, 52246; and 2 Department of Internal Medicine and the Cardiovascular Center, University of Iowa, Iowa City, Iowa 52242

In coronary resistance vessels, endothelium-derived hyperpolarizing factor (EDHF) plays an important role in endothelium-dependent vasodilation. EDHF has been proposed to be formed through cytochrome P-450 monooxygenase metabolism of arachidonic acid (AA). Our hypothesis was that AA-induced coronary microvascular dilation is mediated in part through a cytochrome P-450 pathway. The canine coronary microcirculation was studied in vivo (beating heart preparation) and in vitro (isolated microvessels). Nitric oxide synthase (NOS) (Nomega -nitro-L-arginine, 100 µM) and cyclooxygenase (indomethacin, 10 µM) or cytochrome P-450 (clotrimazole, 2 µM) inhibition did not alter AA-induced dilation. However, when a Ca2+-activated K+ channel channel or cytochrome P-450 antagonist was used in combination with NOS and cyclooxygenase inhibitors, AA-induced dilation was attenuated. We also show a negative feedback by NO on NOS-cyclooxygenase-resistant AA-induced dilation. We conclude that AA-induced dilation is attenuated by cytochrome P-450 inhibitors, but only when combined with inhibitors of cyclooxygenase and NOS. Therefore, redundant pathways appear to mediate the AA response in the canine coronary microcirculation.

coronary circulation; coronary microcirculation; intravital microscopy


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