Role of ATP sensitive potassium channels in long term adaptation to metabolic stress.
Role of ATP sensitive potassium channels in long term adaptation to metabolic stress.
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ATP 敏感钾通道在长期适应代谢应激中的作用。
DOI：
10.1093/cvr/28.6.788
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发表时间：
1994
影响因子：
10.8
通讯作者：
Baghdady,R
中科院分区：
文献类型：
--
作者：
Cameron,JS;Baghdady,R
代谢抑制过程中心脏 KATP 通道的激活与恶性心律失常、心源性猝死、梗塞面积缩小、预处理和收缩能力更快恢复等多种效应有关。鉴于这些不同的后果，以及反复观察到 KATP 电流在各种代谢应激条件下发生改变，确定所描述的变化是否是潜在病理的一部分，或者它们是否反映了保护心脏功能的内源性适应变得越来越重要。我们支持这样的观点，即增强的 KATP 通道在长期代谢抑制过程中本质上发生了改变，至少部分是通过通道对 ATP 敏感性的降低而改变的，并且这种变化在大多数情况下表现为一种适应性机制。慢性缺血环境中通道活性增加可有助于维持静息电位、限制钙流入、保存 [ATP] i 并防止动作电位持续时间过度延长。
Cardiac KATP channel activation during metabolic inhibition has been implicated in effects ranging from malignant arrhythmogenesis and sudden cardiac death to reduction in infarct size, preconditioning, and a more rapid recovery of contractile ability. Given these disparate consequences, and the repeated observation that KATP currents are altered under a wide variety of metabolically stressful conditions, it becomes increasingly more critical to determine whether the changes described are part of the underlying pathology, or whether they reflect an endogenous adaptation to protect cardiac function. We support the view that enhanced KATP channels are intrinsically altered during long term metabolic inhibition, at least in part through a reduction in channel sensitivity to ATP, and that the change manifests itself in most cases as an adaptive mechanism. Increased channel activity in a chronically ischaemic environment could serve to maintain resting potential, limit calcium influx, conserve [ATP] i, and prevent excessive prolongation of action potential duration.