Abstract
Arachidonic acid can be oxidatively metabolized by cytochrome P450 epoxygenase to four regioisomeric epoxyeichosatrienoic acids (5,6-; 8,9-; 11,12-; 14,15-EET), which exhibit vasorelaxant effects in vivo and in vitro with unknown mechanisms. In this study, the patch-clamp method was used to examine the effects of EETs on the Ca 2+-activated K + channel in cells from rabbit portal vein, rat caudal artery, guinea pig aorta and porcine coronary artery. In all four cell types, EETs in the bath activated the K + channel in cell-attached patches by increasing the single channel open-state probability. Potencies of the four EETs did not differ significantly for each cell type. The concentrations for doubling open-state probability were 0.1 μM in portal vein and coronary artery, 0.3–1 μM in aorta and 1–3 μM in caudal artery. In caudal artery cells, K + channel activation by 3 μM 5,6,- and 1 μM 11,12-EET was blocked and reversed by glyburide at 0.5 μM. In aorta, coronary artery, and caudal artery cells, micromolar EETs induced a dose-dependent and reversible augmentation of whole-cell K + current by 50–120% and a 5–12 mV hyperpolarization. EETs on the cytosolic side of inside-out patches produced little or no potentiation of K + channels, implying an interaction of receptor-mediated nature. Thus, EETs may promote vasolidation by functioning as endogenous K + channel openers.
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