Endothelin-1 inhibits inward rectifier potassium channels and activates nonspecific cation channels in cultured endothelial cells.
A predominant inward rectifier and a small outward potassium current were obtained in whole-cell patch-clamp recordings from cultured bovine pulmonary arterial endothelial cells. Application of endothelial-1 (ET-1; 10-100 nmol/l) inhibited the inward rectifier. Washout with bath solution did not recover the current decreased by ET-1. In cell-attached studies, ET-1 (1 nmol/l) inhibited single-channel activity of the inward rectifier and in some patches enhanced activity of the outward potassium current without change of conductance. A non-specific cation current which is permeable to calcium was identified in cell-attached patches in cultured human umbilical vein endothelial cells. ET-1 (1 nmol/l) increased activity of the nonspecific cation channel. ET-1 may increase calcium influx into endothelial cells and promote synthase and release of endothelium-derived factors.
Zhang
H
H
Department of Surgery, University of Chicago, IL 60637.
Inazu
M
M
Weir
B
B
Daniel
E
E
D000818:Animals; D002118:Calcium / Q000502:physiology; D002417:Cattle; D002478:Cells, Cultured; D004594:Electrophysiology; D016232:Endothelins / Q000494:pharmacology*; D004730:Endothelium, Vascular / Q000502:physiology*; D006801:Humans; D007473:Ion Channels / Q000502:physiology*; D008564:Membrane Potentials; D011188:Potassium / Q000502:physiology; D015221:Potassium Channels / Q000187:drug effects* / Q000502:physiology
D016232:Endothelins; D007473:Ion Channels; D015221:Potassium Channels; D011188:Potassium; D002118:Calcium