Pérez G, Toro L
Department of Molecular Physiology and Biophysics, Baylor College of Medicine, Houston 77030.
Am J Physiol. 1994 May;266(5 Pt 1):C1459-63. doi: 10.1152/ajpcell.1994.266.5.C1459.
Uterine excitability depends on ion channel activity, the expression of which is regulated by sexual hormones. We show now that the action of protein kinase A (PKA) on large-conductance calcium-activated K+ (KCa) channel activity also depends on the hormonal status. PKA-dependent phosphorylation of reconstituted KCa channels from midpregnant rats usually stimulated channel activity; in contrast, KCa channels from nonpregnant rat and human myometrium were primarily inhibited by this mechanism. Both effects were reversible by phosphatase treatment. These results suggest that one important factor modulating uterine contractility during pregnancy or the regular cycle may be the differential response of KCa channels toward PKA-induced phosphorylation.
子宫的兴奋性取决于离子通道活性，而离子通道的表达受性激素调控。我们现在发现，蛋白激酶A（PKA）对大电导钙激活钾离子（KCa）通道活性的作用也取决于激素状态。来自妊娠中期大鼠的重组KCa通道的PKA依赖性磷酸化通常会刺激通道活性；相反，来自未孕大鼠和人子宫肌层的KCa通道主要受该机制抑制。两种效应均可通过磷酸酶处理逆转。这些结果表明，在妊娠或正常月经周期中调节子宫收缩性的一个重要因素可能是KCa通道对PKA诱导的磷酸化的不同反应。
