肾上腺素对心肌钙电导的调节
The regulation of the calcium conductance of cardiac muscle by adrenaline.
作者信息
Reuter H, Scholz H
出版信息
J Physiol. 1977 Jan;264(1):49-62. doi: 10.1113/jphysiol.1977.sp011657.
Abstract
- The effect of adrenaline on the Ca-dependent slow inward current, Is, of mammalian cardiac muscle has been investigated by the voltage-clamp method. The mechanism of the increase in the conductance, gs, was analysed on the basis of a kinetic scheme (Hodgkin & Huxley, 1952) applicable to this system. 2. The rate constants alphad and betad, of activation of gs were not influenced by adrenaline, although the limiting conductance, gs, was greatly increased. 3. Reduction of [Ca]o from 1-8 to 0-2 mM decreased the amplitude of inward tail currents when gs was fully activated; however, the relative decrease of the current amplitude was the same with and without adrenaline. The reversal potential, ER, of Is was not changed by the drug. This indicates that the catecholamine has no influence on the selectivity of these conductance channels. 4. An increase in the number of functional conductance channels by adrenaline is discussed as a possible mechanism for the increase in Gs.
摘要
- 采用电压钳法研究了肾上腺素对哺乳动物心肌中钙依赖性慢内向电流Is的影响。基于适用于该系统的动力学模型（Hodgkin和Huxley，1952）分析了电导增加（gs）的机制。2. 尽管极限电导gs大幅增加，但gs激活的速率常数alphad和betad不受肾上腺素影响。3. 当gs完全激活时，将细胞外钙浓度[Ca]o从1.8 mM降至0.2 mM会降低内向尾电流的幅度；然而，有无肾上腺素时电流幅度的相对降低是相同的。药物未改变Is的反转电位ER。这表明儿茶酚胺对这些电导通道的选择性没有影响。4. 讨论了肾上腺素增加功能性电导通道数量作为gs增加的一种可能机制。
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