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Role of calcium and calmodulin in ciliary stimulation induced by acetylcholine.

机译:钙和钙调蛋白在乙酰胆碱诱导的睫状刺激中的作用。

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The goal of this work was to elucidate the molecular events underlying stimulation of ciliary beat frequency (CBF) induced by acetylcholine (ACh) in frog esophagus epithelium. ACh induces a profound increase in CBF and in intracellular Ca(2+) concentration ([Ca(2+)](i)) through M(1) and M(3) muscarinic receptors. The [Ca(2+)](i) slowly decays to the basal level, while CBF stabilizes at an elevated level. These results suggest that ACh triggers Ca(2+)-correlated and -uncorrelated modes of ciliary stimulation. ACh response is abolished by the phospholipase C (PLC) inhibitor U-73122 and by depletion of intracellular Ca(2+) stores but is unaffected by reduction of extracellular Ca(2+) concentration and by blockers of Ca(2+) influx. Therefore, ACh activates PLC and mobilizes Ca(2+) solely from intracellular stores. The calmodulin inhibitors W-7 and calmidazolium attenuate the ACh-induced increase in [Ca(2+)](i) but completely abolish the elevation in CBF. Therefore, elevation of [Ca(2+)](i) is necessary forCBF enhancement but does not lead directly to it. The combined effect of Ca(2+) elevation and of additional factors, presumably mobilized by Ca(2+)-calmodulin, results in a robust CBF enhancement.
机译:这项工作的目的是阐明在青蛙食管上皮中乙酰胆碱(ACh)引起的纤毛跳动频率(CBF)刺激的分子事件。 ACh诱导CBF和细胞内Ca(2+)浓度([Ca(2 +)](i))通过M(1)和M(3)毒蕈碱受体的大幅增加。 [Ca(2 +)](i)缓慢衰减至基础水平,而CBF稳定在升高的水平。这些结果表明乙酰胆碱触发Ca(2 +)-相关和-不相关的睫状刺激模式。 ACh反应被磷脂酶C(PLC)抑制剂U-73122和细胞内Ca(2+)储存耗竭所废除,但不受细胞外Ca(2+)浓度降低和Ca(2+)流入阻滞剂的影响。因此,ACh激活PLC和动员Ca(2+)仅从细胞内的存储。钙调素抑制剂W-7和Calmidazolium减弱了ACh诱导的[Ca(2 +)](i)的增加,但完全消除了CBF的升高。因此,[Ca(2 +)](i)的升高对于CBF增强是必要的,但并不直接导致其升高。 Ca(2+)升高和其他因素的组合效应,大概是由Ca(2 +)-钙调蛋白动员的,导致了强大的CBF增强。

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