Pharmacological modulation of 86Rb efflux from aortic endothelial cells.
The ATP-induced efflux of 86Rb from prelabelled bovine aortic endothelial cells was inhibited by quinine (50 microM) but not by a tetraethylammonium (5 mM) or apamin (50 nM). Neither sulfonylureas nor pinacidil had a significant effect on the rate of 86Rb efflux from the endothelial cells. These data are consistent with the presence of intermediate conductance Ca2(+)-activated K+ channels in endothelial cells. ATP-dependent K+ channels, sensitive to sulfonylureas and pinacidil, could not be detected.
Ramboer
I
I
Institute of Interdisciplinary Research, School of Medicine, Free University of Brussels, Belgium.
Boeynaems
J M
JM
D015121:6-Ketoprostaglandin F1 alpha / Q000378:metabolism; D000818:Animals; D001013:Aorta, Thoracic / Q000166:cytology / Q000187:drug effects; D002121:Calcium Channel Blockers / Q000494:pharmacology; D002417:Cattle; D004730:Endothelium, Vascular / Q000166:cytology / Q000378:metabolism*; D011464:Epoprostenol / Q000096:biosynthesis; D015221:Potassium Channels / Q000187:drug effects; D011453:Prostaglandins / Q000032:analysis; D011863:Radioimmunoassay; D012413:Rubidium / Q000378:metabolism*; D012414:Rubidium Radioisotopes
D002121:Calcium Channel Blockers; D015221:Potassium Channels; D011453:Prostaglandins; D012414:Rubidium Radioisotopes; D015121:6-Ketoprostaglandin F1 alpha; D011464:Epoprostenol; D012413:Rubidium