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Mechanisms underlying varioux regulation of Ca chammel activity in smooty muscle cells

平滑肌细胞 Cachammel 活性的多种调节机制

基本信息

批准号：
04671365
负责人：
IMAIZUMI Yuji
金额：
$ 1.34万
依托单位：
Nagoya City University
依托单位国家：
日本
项目类别：
Grant-in-Aid for General Scientific Research (C)
财政年份：
1992
资助国家：
日本
起止时间：
1992 至 1993
项目状态：
已结题

来源：
https://kaken.nii.ac.jp/en/grant/KAKENHI-PROJECT-04671365/
关键词：
smooth muscle Ca channel noradrenaline arachidonic acid Ca-activated K current sarcoplasmic reticulum cyclopiazonic acid ミクロビアゾン酸 alpha-アドレナリン受容体 α_1-アドレナリン受容体 Ca依在性K電流

项目摘要

This project was undertaken to elucidate the mechanisms underlying variety oof regulation of Ca channel activity in smooth muscle cells. In previous study, we showed that norepinephrine (NE) reduces Ca current via two distinctive mechanisms ; Ca-dependent inactivation of Ca channels and Ca-independent regulation. In the present study, it was found that Ca-dependent inactivation of Ca channels mechanism in response to NE was much less available in ureter smooth muscle cells than in vas deferens in Ca-independent mechanism in two type of cells may be attributable to NE-induced release of arachidonic acid (AA) which may contribute the reduction of Ca current in cells from vas deferens but not from ureter. Although the decrease in Ca current by exogenously applied AA was large in vas deferens cells, it was not clear that the release of AA contributed to the NE-induced decrease in Ca current. The AA-induced decrease in Ca current was not affected by treatment with inhibitors of cycloxygenas … More e and lipoxygenase. The decrease was. however, partly inhibited by superoxide desmutase, indicating involvement of superoxide anion production from AA.Moreover, it became clear that NE reduced Ca-activated K current more extensively than Ca current. This resulted in the prolongation of action potentiol duration and the potentiation of contraction.The possibility was also examined that the Ca channel activity is increased by significant decrease in atored Ca in the cell after large release. It was found that memvrane excitability was increased and action potentials were more frequently generated after treatment with cyclopiazonic acid which is a novel inhibitor of Ca-pump in sarcoplasmic reticulum. The major mechanism for the CPA-induced change was the inhibition of Ca-activated K current. Although direct evidence indication ghat depletion of intracellular Ca storage sites results in the potentiation of Ca channel activity was not obtained, the possibility is also likely and may contribute to the increase in membrane excitabilyty. Less

本研究旨在阐明不同钙通道活性调控的机制。在以前的研究中，我们发现去甲肾上腺素(NE)通过两种不同的机制来减少钙电流：钙依赖的钙通道失活和钙非依赖性的调节。本研究发现，去甲肾上腺素引起的输尿管平滑肌细胞钙通道失活机制比输精管细胞的钙通道失活机制要弱得多，这两种细胞的钙非依赖性机制可能归因于去甲肾上腺素诱导的花生四烯酸(AA)的释放，这可能是由于去甲肾上腺素导致输精管细胞钙电流的减少，而不是输尿管细胞钙电流的减少。尽管外源性AA对输精管细胞的钙电流有较大的抑制作用，但AA的释放是否参与了去甲肾上腺素引起的钙电流的降低尚不清楚。环氧合酶…抑制剂不影响AA引起的钙电流降低更多的E和脂氧合酶。减少的是。但部分地被超氧化物歧化酶抑制，表明AA参与了超氧阴离子的产生。此外，NE明显比钙电流更广泛地抑制钙激活的钾电流。这导致了动作电位时程的延长和收缩的增强。还研究了在大量释放后，细胞内钙离子显著减少而导致钙通道活动增加的可能性。研究发现，肌浆网钙泵的新型阻断剂--环匹阿松酸处理后，膜的兴奋性增强，动作电位的产生频率增加。CPA引起的改变的主要机制是抑制钙激活的钾电流。虽然没有直接证据表明细胞内钙存储位点的缺失导致钙通道活性的增强，但这种可能性也是可能的，并可能与膜的兴奋性增加有关。较少