Hu S L, Kim H S, Jeng A Y
Research Department, Ciba-Geigy Corp., Summit, NJ 07901.
Eur J Pharmacol. 1991 Feb 26;194(1):31-6. doi: 10.1016/0014-2999(91)90120-f.
The effects of endothelin-1 (ET-1) on the activity of the large Ca2(+)-activated K+ channel (BK channel) in enzymatically dissociated smooth muscle cells of porcine coronary artery were studied with the cell-attached patch-clamp technique. ET-1 at concentrations between 0.1 and 10 nM potentiated the BK channel activity. This effect was maximal at 1 nM ET-1, resulting in an average of 4.2-fold increase in channel open-state probability as compared with control. ET-1 at concentrations higher than 10 nM produced an irreversible inhibition of the BK channel activity, primarily due to a marked decrease in the channel mean open-time. The activation by lower doses of ET-1, but not the inhibition by higher doses of ET-1, of the BK channel was blocked by 0.1 microM PN 200-110, a Ca2+ channel blocker. The modulation of the BK channel activity in smooth muscle cell membrane may be a possible mechanism for ET-induced vasodilator and vasoconstrictor actions.
采用细胞贴附式膜片钳技术，研究了内皮素-1（ET-1）对猪冠状动脉酶解平滑肌细胞中大电导钙激活钾通道（BK通道）活性的影响。浓度在0.1至10 nM之间的ET-1增强了BK通道活性。该效应在1 nM ET-1时最大，与对照组相比，通道开放概率平均增加了4.2倍。浓度高于10 nM的ET-1对BK通道活性产生不可逆抑制，主要是由于通道平均开放时间显著缩短。低剂量ET-1对BK通道的激活作用（而非高剂量ET-1的抑制作用）被0.1 μM钙通道阻滞剂PN 200-110阻断。平滑肌细胞膜上BK通道活性的调节可能是ET诱导血管舒张和血管收缩作用的一种可能机制。
