Dora Kim A
Department of Pharmacology, University of Oxford, Oxford, UK.
Microcirculation. 2016 Nov;23(8):626-630. doi: 10.1111/micc.12322.
The SMCs of skeletal muscle arterioles are intricately sensitive to changes in membrane potential. Upon increasing luminal pressure, the SMCs depolarize, thereby opening VDCCs, which leads to contraction. Mechanisms that oppose this myogenic tone can involve voltage-dependent and independent dilator pathways, and can be endothelium-dependent or independent. Of particular interest are the pathways leading to hyperpolarization of SMCs, as these can potentially evoke both local and conducted dilation. This review focuses on three agonists that cause local and conducted dilation in skeletal muscle: ACh, ATP, and KCl. The mechanisms for the release of these agonists during motor nerve stimulation and/or hypoxia, and their actions to open either Ca -activated K channels (K ) or inwardly rectifying K channels (K ) are described. By causing local and conducted dilation, each agonist has the ability to improve skeletal muscle blood flow during exercise and ischemia.
骨骼肌小动脉的平滑肌细胞对膜电位变化极为敏感。随着管腔内压力升高，平滑肌细胞去极化，从而打开电压依赖性钙通道（VDCCs），导致收缩。对抗这种肌源性张力的机制可涉及电压依赖性和非依赖性舒张途径，且可为内皮依赖性或非依赖性。特别值得关注的是导致平滑肌细胞超极化的途径，因为这些途径可能引发局部和传导性舒张。本综述聚焦于三种可在骨骼肌中引起局部和传导性舒张的激动剂：乙酰胆碱（ACh）、三磷酸腺苷（ATP）和氯化钾（KCl）。描述了这些激动剂在运动神经刺激和/或缺氧期间释放的机制，以及它们打开钙激活钾通道（KCa）或内向整流钾通道（Kir）的作用。通过引起局部和传导性舒张，每种激动剂都有能力在运动和缺血期间改善骨骼肌血流。
