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Vol. 304, Issue 1, 139-144, January 2003
Department of Physiology and Pharmacology, Wake Forest University
School of Medicine, Winston-Salem, North Carolina (A.W.M., C.D.T.,
D.W.B.); and Department of Internal Medicine, University of Iowa
College of Medicine, Iowa City, Iowa (P.V.G.K., H.C.L., N.L.W.)
We examined the mechanism of arachidonic acid-induced vasodilation in
rat small mesenteric arteries and determined the primary arachidonic
acid metabolites produced by these arteries. Responses to arachidonic
acid in small mesenteric arteries from Sprague-Dawley rats were
investigated in vitro in the presence or absence of endothelium or
after pretreatment with inhibitors of nitric oxide (NO),
cyclooxygenase, cytochrome P450, lipoxygenase, or K+
channels. In addition, the metabolism of arachidonic acid was examined
by incubating arteries with [3H]arachidonic acid in the
presence and absence of cyclooxygenase, cytochrome P450, or
lipoxygenase inhibitors. Finally, the vascular response to both
12(S)-hydroxyeicosatetraenoic acid (HETE) and 12(S)-hydroperoxyeicosatetraenoic acid (HPETE) was
determined. Arachidonic acid induced an endothelium-dependent
vasodilation that was abolished by lipoxygenase inhibitors
[cin-namyl-3,4-dihydroxy-cyanocinnamate (CDC) or 5,8,11-eicosatriynoic
acid (ETI)] and KCl, whereas it was partially inhibited by either
tetraethylammonium or iberiotoxin. In contrast, neither NO nor
cytochrome P450 enzyme inhibitors affected arachidonic acid-mediated
dilation, whereas inhibition of cyclooxygenase enhanced dilation.
Biochemical analysis revealed that small mesenteric arteries primarily
produce 12-HETE, a lipoxygenase metabolite. Moreover, CDC and ETI
inhibited the production of 12-HETE. Finally, both
12(S)-HETE and 12(S)-HPETE induced a
concentration-dependent vasodilation in mesenteric arteries. These
findings provide functional and biochemical evidence that the
lipoxygenase pathway mediates arachidonic acid-induced
vasodilation in rat small mesenteric arteries through a K+
channel-dependent mechanism.
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