Zhou Y Y, Yao J A, Tseng G N
Department of Pharmacology, Columbia University, New York, NY 10032, USA.
Pflugers Arch. 1997 Apr;433(6):750-7. doi: 10.1007/s004240050341.
We studied the effects of cell swelling on membrane currents of canine ventricular myocytes using the whole-cell patch-clamp method. Cell swelling was induced by lowering the osmolarity of the bath solution to 60% of control. Cell width and currents were measured simultaneously. Cell swelling induced little or no change in the L-type Ca, the inward rectifier, and the transient outward currents, but a marked increase in the slow delayed rectifier current (IKs) was seen. We further examined the role of protein kinase activities in IKs modulation by cell swelling. This modulation was not affected by inhibiting serine/threonine kinases using H-8. On the other hand, the modulation was inhibited by genistein (a protein tyrosine kinase inhibitor) although not by daidzein (an inactive analogue of genistein). Our data suggest that in canine ventricle cell swelling can increase protein tyrosine kinase activity, which can augment IKs and contribute to changes in membrane electrical activity observed under these conditions.
我们使用全细胞膜片钳方法研究了细胞肿胀对犬心室肌细胞膜电流的影响。通过将浴液渗透压降至对照的60%来诱导细胞肿胀。同时测量细胞宽度和电流。细胞肿胀对L型钙电流、内向整流电流和瞬时外向电流几乎没有影响或没有影响，但观察到缓慢延迟整流电流（IKs）显著增加。我们进一步研究了蛋白激酶活性在细胞肿胀调节IKs中的作用。使用H-8抑制丝氨酸/苏氨酸激酶不会影响这种调节。另一方面，金雀异黄素（一种蛋白酪氨酸激酶抑制剂）可抑制这种调节，而大豆苷元（金雀异黄素的无活性类似物）则不会。我们的数据表明，在犬心室中，细胞肿胀可增加蛋白酪氨酸激酶活性，这可增强IKs并导致在这些条件下观察到的膜电活动变化。
