Key result
Endothelin blocks coronary K-ATP channels and induces smooth muscle depolarization at ~1.3 nM concentrations.
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ATP-sensitive K+ channels with a conductance of 30 pS in smooth muscle cells of porcine coronary artery were found to be highly active in the intact cell-attached patch configuration when the pipette contained a physiological concentration of Ca2+ (greater than 10(-4) M). In the inside-out configuration, these channels were activated by extracellular Ca2+ and blocked by cytosolic ATP and glibenclamide. Endothelin applied to the pipette specifically blocked these channels in a concentration-dependent manner in the cell-attached configuration (half-maximal inhibition, 1.3 x 10(-9) M). A K+ channel opener, nicorandil, activated these channels even in the presence of 10(-8) M endothelin. In the whole-cell current-clamp method, the cell membrane was depolarized by endothelin and then repolarized by nicorandil. The membrane depolarization is closely related to contraction of smooth muscle cells. These results suggest that the ATP-sensitive K+ channels are important in controlling the vascular tone of the coronary artery and that endothelin can increase vascular tone by blocking these channels.
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Miyoshi et al. (1992) studied Vascular tone regulation in porcine coronary artery smooth muscle cells. Endothelin vs. Nicorandil (K+ channel opener) was evaluated on Inhibition of 30 pS ATP-sensitive K+ channels and membrane depolarization (IC50 1.3 x 10^-9 M). Endothelin blocked 30 pS ATP-sensitive K+ channels in porcine coronary smooth muscle cells in a concentration-dependent manner (half-maximal inhibition 1.3 x 10^-9 M) and caused depolarization.
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