Regulation of Potassium Channels in Coronary Arterial Smooth Muscle by Endothelium-Derived Vasodilators

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Abstract
Recent studies have suggested that coronary endothelial cells produce and release nitric oxide (NO), prostaglandin I 2 , and epoxyeicosatrienoic acids (EETs). These endothelium-derived vasodilators play an important role in the control of coronary vascular tone. However, the mechanism by which these endothelium-derived vasodilators cause relaxation of coronary arterial smooth muscle has yet to be determined. This study characterized and compared the effects of NO, prostaglandin I 2 , and 11,12-EET on the two main types of potassium channels in small bovine coronary arterial smooth muscle: the large conductance Ca 2+ -activated K + channels (K Ca ) and 4-aminopyridine-sensitive delayed rectifier K + channels (K drf ). In cell-attached patches, non-oate, an NO donor, activated both K Ca and K drf channels. The open probability of both K Ca and K drf channels increased 10- to 25-fold when nonoate was added to the bath at concentrations of 10 −6 to 10 −4 mol/L. 11,12-EET (10 −8 to 10 −4 mol/L) also increased the activity of the K Ca channels in a concentration-dependent manner, but it had no effect on the activity of the K drf channels, even in the highest concentration studied (10 −4 mol/L). In contrast to the effect of 11,12-EET, iloprost, a prostaglandin I 2 analogue (10 −6 to 10 −4 mol/L), produced a concentration-dependent increase in the activity of K drf channels without affecting the K Ca channels. In conclusion, all three endothelium-derived vasodilators act to open potassium channels; however, the channel types that they affect are different. NO activates both K Ca and K drf channels; 11,12-EET activates only the K Ca channels; and prostaglandin I 2 activates only the K drf channels.

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