Shimamura K, Kusaka M, Sperelakis N
Department of Molecular and Cellular Physiology, College of Medicine, University of Cincinnati, OH 45267-0576, USA.
Can J Physiol Pharmacol. 1994 Nov;72(11):1304-7. doi: 10.1139/y94-187.
The factors that regulate the voltage-dependent Ca2+ channels in pregnant uterine smooth muscle cells have not been elucidated, including any roles for protein kinase C (PKC). Therefore, the role of PKC in the regulation of the slow (L type) Ca2+ channels was examined in myometrial cells isolated from late pregnant (18-19 day) rat uterus, using the nystatin-perforated whole-cell voltage clamp. A PKC activator, phorbol 12,13-dibutyrate (PDB), increased the L-type Ca2+ current (ICa(L)). Bath application of PDB (0.03 and 0.3 microM) increased the peak amplitude of ICa(L) by 21 +/- 14% (n = 6) and 37 +/- 8% (n = 9, p < 0.01), respectively. PDB did not change the holding current or shift the current-voltage relationship for ICa(L). The PKC inhibitors, H-7 (20 microM) or staurosporine (10 nM), reversed the effect of PDB. These results indicate that PKC may play a role in regulating Ca2+ channel function in pregnant rat myometrial cells and, therefore, may be involved in control of uterine contraction.
调节妊娠子宫平滑肌细胞中电压依赖性Ca2+通道的因素尚未阐明，包括蛋白激酶C（PKC）的任何作用。因此，使用制霉菌素穿孔全细胞电压钳，在从妊娠晚期（18 - 19天）大鼠子宫分离的子宫肌层细胞中研究了PKC在调节慢（L型）Ca2+通道中的作用。PKC激活剂佛波醇12,13 - 二丁酸酯（PDB）增加了L型Ca2+电流（ICa(L)）。浴槽应用PDB（0.03和0.3 microM）分别使ICa(L)的峰值幅度增加了21 +/- 14%（n = 6）和37 +/- 8%（n = 9，p < 0.01）。PDB没有改变钳制电流或移动ICa(L)的电流 - 电压关系。PKC抑制剂H - 7（20 microM）或星形孢菌素（10 nM）逆转了PDB的作用。这些结果表明，PKC可能在调节妊娠大鼠子宫肌层细胞的Ca2+通道功能中起作用，因此可能参与子宫收缩的控制。
