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Vol. 287, Issue 2, 497-503, November 1998
Department of Cell Biology, UMDNJ-SOM, Stratford, New Jersey (J.Q.)
and
Department of Pharmacology, New York Medical College,
Valhalla, New York (D.F., J.C.M.)
A cytochrome P450-derived metabolite of arachidonic acid, namely
an epoxyeicosatrienoic acid (EET), has many of the properties of a
hyperpolarizing factor that mediates endothelium-dependent, nitric
oxide-independent vasodilation. As there are four EET regioisomers, we
used pharmacological criteria, based on previous observations with
bradykinin (BK), to evaluate which, if any, of the EETs could be
considered a potential mediator of vasodilator responses to BK in the
rat isolated heart treated with indomethacin and nitroarginine to
eliminate prostaglandin and nitric oxide components of the response.
Nifedipine, used as a probe for dilator mechanisms dependent on closure
of voltage-dependent Ca++ channels, almost abolished the
vasodilator effect of cromakalim and attenuated those of BK and 5,6 EET. The vasodilator effects of the other EETs were not reduced and
were excluded from consideration as mediators of BK-induced
vasodilation. The vasodilator effect of 5,6 EET, as with that of BK,
was markedly reduced by charybdotoxin but not iberiotoxin, suggesting
the contribution of a similar type K+ channel to the
vascular response to both agents. As expected for a putative
endothelium- and cytochrome P450-derived mediator, the coronary
vasodilator effect of 5,6 EET was not affected by either removal of the
endothelium or inhibition of cytochrome P450 with clotrimazole,
interventions that virtually abolished the vasodilator activity of BK.
Thus, of the four EET regioisomers, 5,6 EET is the most likely mediator
of the vasodilator effect of BK in the isolated heart under these
experimental conditions.
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