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Mechanisms of myogenic response: Ca2+-dependent and -independent signaling

机译:成肌反应的机制:Ca 2 + 依赖性和非依赖性信号传导

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In many organs, blood flow is maintained at a relatively constant level although pressure changes substantially. This autoregulation of blood flow is achieved in several ways including the myogenic response (MR). MR is triggered by mechanical stretch of vascular smooth muscle. Activation of stretch activated channels (SACs) on vascular smooth muscle cells induces depolarization, Ca2+ influx and myogenic constriction. Non-selective cation channel, epithelial Na+ channel, chloride channel and potassium channel have been suggested as a molecular candidate of SAC. Additionally, activation of protein kinase C (PKC) and Rho-A kinase (ROK) contribute to MR without alteration of intracellular Ca2+. These complex interactions of Ca2+-dependent and Ca2+-sensitizing signals seem to be variable depending on the types of arteries as well as animal species. Finally, impaired MRs are related in various pathological conditions, such as hypertension, stroke and diabetes mellitus. Therefore, identification of MR signaling mechanism might be a target of treatment in vascular diseases.
机译:在许多器官中,尽管压力发生很大变化,但血流仍保持在相对恒定的水平。血流的这种自动调节可以通过多种方式实现,包括肌源性反应(MR)。 MR是由血管平滑肌的机械拉伸触发的。血管平滑肌细胞上的拉伸激活通道(SAC)的激活引起去极化,Ca 2 + 大量涌入和肌源性收缩。非选择性阳离子通道,上皮Na + 通道,氯离子通道和钾通道被认为是SAC的分子候选物。此外,蛋白激酶C(PKC)和Rho-A激酶(ROK)的激活对MR有贡献,而胞内Ca 2 + 却没有改变。 Ca 2 + 依赖性和Ca 2 + 致敏信号的这些复杂的相互作用似乎取决于动脉的类型和动物种类而变化。最后,受损的MR与各种病理状况有关,例如高血压,中风和糖尿病。因此,MR信号机制的鉴定可能是血管疾病的治疗目标。

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