THE EFFECTS OF RACEMIC, (-PINACIDIL AND (-)-PINACIDIL ON THE MEMBRANE-POTENTIAL OF THE RAT AORTA())

The endothelium-intact and -denuded rat aorta is hyperpolarized by rac emic and (-)-pinacidil, probably by opening ATP-dependent potassium ch annels. (+)-Pinacidil caused depolarization of the endothelium-intact and -denuded rat aorta. The depolarization induced by 20 mM KCl in the endothelium-intact rat aorta was reversed by racemic and (-)-, but no t by (+)-pinacidil. On the endothelium-intact rat aorta, isoprenaline produced hyperpolarization and ICI 118551 7-methylindan-4-yloxy)-3-iso propylaminobutan-2-ol) had no effect alone but prevented isoprenaline from causing hyperpolarization. The hyperpolarization induced by isopr enaline was reversed by racemic and (+)-, but not by (-)-pinacidil. Gl ibenclamide depolarized the endothelium-intact rat aorta and prevented the hyperpolarizing action of racemic pinacidil and (-)-pinacidil. ()-Pinacidil prevented the hyperpolarizing action of (-)-pinacidil. Gli benclamide is probably preventing the hyperpolarization associated wit h opening of the ATP-dependent potassium channel by blocking this chan nel. Several mechanisms may underlie the depolarizing action of (+)-pi nacidil, including blocking of ATP-dependent potassium channels.