Publication Type:Journal Article
Source:J Hypertens Suppl, Volume 8, Issue 7, p.S193-201 (1990)
The contribution of Ca2(+)-dependent K+ [K(Ca2+)] channels to the electrical response of cultured bovine aortic endothelial cells following bradykinin stimulation was investigated using the patch-clamp method in the cell-attached configuration. Results indicate (1) that bradykinin activates a voltage-insensitive K(Ca2+) channel of 40 pS in 150 mmol/l KCl through a second messenger mechanism; (2) that the time-course of the K(Ca2+) channel activation process corresponds to the time-dependent changes in cytosolic Ca2+ triggered by bradykinin; and (3) that there is a direct correlation between the cellular hyperpolarization induced by bradykinin and the activation of the K(Ca2+) channels. It is proposed that the hyperpolarization of bovine aortic endothelial cells following bradykinin stimulation is a result of the activation of K(Ca2+) channels, and not of a modification in the gating behaviour of an inward rectifying K+ channel (lk1) that is also observed in these cells. A more negative membrane potential may, in turn, enhance the Ca2+ influx involved in the bradykinin-induced Ca2+ signalling process.