Bradykinin-induced potassium current in cultured bovine aortic endothelial cells.

Bovine aortic endothelial cells (BAECs) respond to bradykinin with an increase in cytosolic-free Ca2+ concentration, [Ca2+]i, accompanied by an increase in surface membrane K+ permeability. In this study, electrophysiological measurement of K+ current was combined with 86Rb+ efflux measurements to characterize the K+ flux pathway in BAECs. Bradykinin- and Ca2(+)-activated K+ currents were identified and shown to be blocked by the alkylammonium compound, tetrabutylammonium chloride and by the scorpion toxin, noxiustoxin, but not by apamin or tetraethylammonium chloride. Whole-cell and single-channel current analysis suggest that the threshold for Ca2+ activation is in the range of 10 to 100 nM [Ca2+]i. The whole-cell current measurements show voltage sensitivity only at the membrane potentials more positive than 0 mV where significant current decay occurs during a sustained depolarizing pulse. Another K+ current present in control conditions, an inwardly rectifying K+ current, was blocked by Ba2+ and was not affected by noxiustoxin or tetrabutylammonium chloride. Efflux of 86Rb+ from BAEC monolayers was stimulated by both bradykinin and ionomycin. Stimulated efflux was blocked by tetrabutyl- and tetrapentyl-ammonium chloride and by noxiustoxin, but not by apamin or furosemide. Thus, 86Rb+ efflux stimulated by bradykinin and ionomycin has the same pharmacological sensitivity as the bradykinin- and Ca2(+)-activated membrane currents. The results confirm that bradykinin-stimulated 86Rb+ efflux occurs via Ca2(+)-activated K+ channels. The blocking agents identified may provide a means for interpreting the role of the Ca2(+)-activated K+ current in the response of BAECs to bradykinin.