Key result
This review describes the mechanisms by which ACh, ATP, and KCl cause local and conducted dilation in skeletal muscle, potentially improving blood flow during exercise and ischemia.
This review highlights the mechanisms by which ACh, ATP, and KCl induce hyperpolarization and dilation in skeletal muscle arterioles, improving blood flow during exercise and ischemia.
Highlights endothelial-smooth muscle interactions in skeletal muscle blood flow; extends mechanistic insights but leaves open clinical translation.
The SMC s of skeletal muscle arterioles are intricately sensitive to changes in membrane potential. Upon increasing luminal pressure, the SMC s depolarize, thereby opening VDCC s, 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 SMC s, 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: AC h, ATP , and KC l. The mechanisms for the release of these agonists during motor nerve stimulation and/or hypoxia, and their actions to open either Ca 2+ ‐activated K + channels ( K C a ) or inwardly rectifying K + channels ( K IR ) are described. By causing local and conducted dilation, each agonist has the ability to improve skeletal muscle blood flow during exercise and ischemia.
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Kim A. Dora (2016) conducted a review in Regulation of vascular tone in skeletal muscle. ACh, ATP, and KCl was evaluated. This review describes the mechanisms by which ACh, ATP, and KCl cause local and conducted dilation in skeletal muscle, potentially improving blood flow during exercise and ischemia.
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