Xiong Z, Burnette E, Cheung D W
University of Ottawa Heart Institute, Canada.
Eur J Pharmacol. 1995 Jul 18;290(2):117-23. doi: 10.1016/0922-4106(95)90023-3.
The effects of the tyrosine kinase inhibitors genistein, lavendustin A, and tyrphostin A25 on Ca(2+)-activated K+ channel activities in freshly isolated single vascular smooth muscle cells from the rat tail artery were studied by patch clamp recording technique. Genistein (5-50 microM) and lavendustin A (10 microM) increased whole-cell Ca(2+)-activated K+ channel currents. Increase in single channel activities by genistein and lavendustin A was also observed in excised inside-out patches. Diadzein (15 microM), an inactive analogue of genistein, did not alter channel activities. Tyrphostin A25 (10 nM), which had no significant effect on whole-cell currents in concentrations up to 50 microM, increased the open probability of the channels by 841% in inside-out patches. No potentiation of whole-cell and single channel activities by genistein was observed when ATP was omitted from the intracellular solutions. These observations suggest that tyrosine kinase modulates Ca(2+)-activated K+ channel activities in vascular smooth muscle cells.
采用膜片钳记录技术，研究了酪氨酸激酶抑制剂染料木黄酮、拉文达ustin A和 tyrphostin A25对大鼠尾动脉新鲜分离的单个血管平滑肌细胞中Ca(2+)激活的K+通道活性的影响。染料木黄酮（5 - 50 microM）和拉文达ustin A（10 microM）增加了全细胞Ca(2+)激活的K+通道电流。在切除的内向外膜片中也观察到染料木黄酮和拉文达ustin A使单通道活性增加。染料木黄酮的无活性类似物黄豆苷元（15 microM）未改变通道活性。Tyrphostin A25（10 nM）在浓度高达50 microM时对全细胞电流无显著影响，但在内向外膜片中使通道的开放概率增加了841%。当细胞内溶液中省略ATP时，未观察到染料木黄酮对全细胞和单通道活性的增强作用。这些观察结果表明酪氨酸激酶调节血管平滑肌细胞中Ca(2+)激活的K+通道活性。
