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Articles in PresS, published online ahead of print March 29, 2002
Am J Physiol Lung Cell Mol Physiol, 10.1152/ajplung.00444.2001
Submitted on November 16, 2001
Accepted on March 24, 2002
* To whom correspondence should be addressed. E-mail: mfuloria{at}wfubmc.edu.
The role of epoxyeicosatrienoic acids in the modulation of neonatal pulmonary vascular tone remains unexplored. We examined the responses of newborn piglet pulmonary resistance arteries (PRAs) to 5,6-epoxyeicosatrienoic acid (5,6-EET), a cytochrome P450 metabolite of arachidonic acid. In PRAs preconstricted with a thromboxane A2 mimetic, 5,6-EET caused a concentration-dependent dilation. This dilation was partially inhibited by the combination of charybdotoxin (CTX) and apamin, inhibitors of large and small conductance calcium-dependent potassium (KCa) channels and was abolished by depolarization of vascular smooth muscle with KCl. Disruption of the endothelium significantly attenuated the dilation, suggesting involvement of one or more endothelium-derived vasodilator pathways in this response. The dilation was partially inhibited by nitro-L-arginine (L-NA), an inhibitor of nitric oxide synthase (NOS) but was unaffected by indomethacin, a cyclooxygenase (COX) inhibitor. The combined inhibition of NOS and KCa channels with L-NA, CTX and apamin abolished 5,6-EET-mediated dilation. Similarly, combined inhibition of NOS and COX abolished the response. We conclude that 5,6-EET is a potent vasodilator in newborn piglet PRAs. This dilation is mediated by redundant pathways that include release of nitric oxide (NO) and COX metabolites, and activation of KCa channels. The endothelium-dependence of this response suggests that 5,6-EET is not itself an endothelium-derived hyperpolarizing factor (EDHF) but may induce the release of one or more endothelium-derived relaxing factors, such as NO and/or EDHF.
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