CYCLIC-AMP AND PHOSPHORYLATION IN REGULATION OF CA++ INFLUX INTO MYOCARDIAL-CELLS AND BLOCKADE BY CALCIUM ANTAGONISTIC DRUGS
CYCLIC-AMP AND PHOSPHORYLATION IN REGULATION OF CA++ INFLUX INTO MYOCARDIAL-CELLS AND BLOCKADE BY CALCIUM ANTAGONISTIC DRUGS
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DOI：
10.1016/0002-8703(84)90385-5
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发表时间：
1984-01-01
影响因子：
4.8
通讯作者：
SPERELAKIS, N
中科院分区：
文献类型：
--
作者：
SPERELAKIS, N
环磷酸腺苷（AMP）在控制心脏Ca++慢通道中的作用常常被忽视。本文就心肌慢通道的一些重要特性，特别是环腺苷酸对慢通道的调节作一简要综述。此外，将简要讨论慢动作电位（AP）、钙拮抗剂的作用机制以及慢AP在心律失常中的可能作用。心脏的收缩力由兴奋-收缩偶联过程中AP期间跨细胞膜的Ca++内流控制。这种Ca++内流通过细胞膜的电压依赖性和时间依赖性门控慢通道发生。还有其他类型的电压依赖性通道，包括快速Nat通道和几种类型的K+通道。每种类型的离子通道都是一种特定的蛋白质，漂浮在细胞膜的脂质双层基质中，具有充满水的中心孔用于离子通过。通过离子选择性通道的阳离子可能在其通过通道的电化学（电加浓度）梯度的过程中与两个或三个带负电荷的位点结合。快Nat通道和慢通道在膜的内表面具有中心激活（A、m或d）门和失活（I、h或f）门。
The role of cyclic adenosine monophosphate (AMP) in controlling the availability of Ca++ slow channels in the heart is often overlooked. The purpose of this article is to briefly review and summarize some of the important properties of the myocardial slow channels, particularly their regulation by cyclic AMP. In addition, the slow action potentials (APs), the mechanisms of action of the calcium antagonistic drugs, and the possible role of slow APs in cardiac arrhythmias will be discussed briefly. The force of contraction of the heart is controlled by the Ca++ influx across the cell membrane during the AP, in the process of excitation-contraction coupling. This Ca++ influx occurs through the voltage-dependent and time-dependent gated slow channels of the cell membrane. There are other types of voltage-dependent channels, including fast Nat channels and several types of K+ channels. Each type of ionic channel is a specific protein that floats in the lipid bilayer matrix of the cell membrane, with a water-filled central pore for ion passage. A cation passing through its ion-selective channel probably binds to two or three negatively charged sites on its journey through the channel down its electrochemical (electrical plus concentration) gradient. The fast Nat channels and the slow channels have a central activation (A, m, or d) gate and an inactivation (I, h, or f) gate at the inner surface of the membrane.