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首页> 外文期刊>American Journal of Physiology >Regulation of smooth muscle calcium sensitivity: KCl as a calcium-sensitizing stimulus.
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Regulation of smooth muscle calcium sensitivity: KCl as a calcium-sensitizing stimulus.

机译：调节平滑肌钙敏感性：KCl作为钙敏感性刺激物。

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KCl has long been used as a convenient stimulus to bypass G protein-coupled receptors (GPCR) and activate smooth muscle by a highly reproducible and relatively "simple" mechanism involving activation of voltage-operated Ca2+ channels that leads to increases in cytosolic free Ca2+ ([Ca2+]i), Ca2+-calmodulin-dependent myosin light chain (MLC) kinase activation, MLC phosphorylation and contraction. This KCl-induced stimulus-response coupling mechanism is a standard tool-set used in comparative studies to explore more complex mechanisms generated by activation of GPCRs. One area where this approach has been especially productive is in studies designed to understand Ca2+ sensitization, the relationship between [Ca2+]i and force produced by GPCR agonists. Studies done in the late 1980s demonstrated that a unique relationship between stimulus-induced [Ca2+]i and force does not exist: for a given increase in [Ca2+]i, GPCR activation can produce greater force than KCl, and relaxant agents can produce the opposite effect to cause Ca2+ desensitization. Such changes in Ca2+ sensitivity are now known to involve multiple cell signaling strategies, including translocation of proteins from cytosol to plasma membrane, and activation of enzymes, including RhoA kinase and protein kinase C. However, recent studies show that KCl can also cause Ca2+ sensitization involving translocation and activation of RhoA kinase. Rather than complicating the Ca2+ sensitivity story, this surprising finding is already providing novel insights into mechanisms regulating Ca2+ sensitivity of smooth muscle contraction. KCl as a "simple" stimulus promises to remain a standard tool for smooth muscle cell physiologists, whose focus is to understand mechanisms regulating Ca2+ sensitivity.
机译：长期以来，氯化钾一直被用作绕过G蛋白偶联受体（GPCR）的便利刺激物，并通过高度可复制且相对“简单”的机制激活平滑肌，该机制涉及激活电压操作的Ca2 +通道，从而导致细胞质游离Ca2 +（ [Ca2 +] i），Ca2 +-钙调蛋白依赖性肌球蛋白轻链（MLC）激酶激活，MLC磷酸化和收缩。这种由KCl诱导的刺激反应耦合机制是在比较研究中探索由GPCR激活产生的更复杂机制的标准工具集。该方法特别有效的一个领域是旨在了解Ca2 +致敏作用，[Ca2 +] i与GPCR激动剂产生的力之间关系的研究。 1980年代后期进行的研究表明，刺激诱导的[Ca2 +] i与作用力之间不存在独特的关系：对于[Ca2 +] i的给定增加，GPCR活化作用可产生比KCl更大的作用力，而松弛剂则可产生作用力。引起Ca2 +脱敏的相反作用。现在已知，Ca2 +敏感性的这种变化涉及多种细胞信号传导策略，包括蛋白质从胞质溶胶转移到质膜，以及酶的激活，包括RhoA激酶和蛋白激酶C。但是，最近的研究表明，KCl也可以引起Ca2 +致敏涉及RhoA激酶的易位和激活。并非使Ca2 +敏感性的故事复杂化，这一令人惊讶的发现已经为调节平滑肌收缩的Ca2 +敏感性的机制提供了新颖的见解。 KCl作为一种“简单”的刺激方法，有望成为平滑肌细胞生理学家的标准工具，其重点是了解调节Ca2 +敏感性的机制。

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