Walsh K B, Kass R S
Department of Physiology, University of Rochester, School of Medicine and Dentistry, NY 14642.
Science. 1988 Oct 7;242(4875):67-9. doi: 10.1126/science.2845575.
The enzymes adenosine 3',5'-monophosphate (cAMP)-dependent protein kinase (protein kinase A) and protein kinase C regulate the activity of a diverse group of cellular proteins including membrane ion channel proteins. When protein kinase A was stimulated in cardiac ventricular myocytes with the membrane-soluble cAMP analog 8-chlorphenylthio cAMP (8-CPT cAMP), the amplitude of the delayed-rectifier potassium current (IK) doubled when recorded at 32 degrees C but was not affected at 22 degrees C. In contrast, modulation of the calcium current (ICa) by 8-CPT cAMP was independent of temperature with similar increases in ICa occurring at both temperatures. Stimulation of protein kinase C by phorbol 12,13-dibutyrate also enhanced IK in a temperature-dependent manner but failed to increase ICa at either temperature. Thus, cardiac delayed-rectifier potassium but not calcium channels are regulated by two distinct protein kinases in a similar temperature-dependent fashion.
腺苷3',5'-单磷酸（cAMP）依赖性蛋白激酶（蛋白激酶A）和蛋白激酶C可调节包括膜离子通道蛋白在内的多种细胞蛋白的活性。当用膜溶性cAMP类似物8-氯苯基硫代cAMP（8-CPT cAMP）刺激心室肌细胞中的蛋白激酶A时，在32℃记录时延迟整流钾电流（IK）的幅度增加了一倍，但在22℃时不受影响。相比之下，8-CPT cAMP对钙电流（ICa）的调节与温度无关，在两个温度下ICa均有类似增加。佛波醇12,13-二丁酸酯对蛋白激酶C的刺激也以温度依赖性方式增强了IK，但在任一温度下均未增加ICa。因此，心脏延迟整流钾通道而非钙通道以类似的温度依赖性方式受到两种不同蛋白激酶的调节。
