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首页> 外文期刊>Journal of Cellular Physiology >Agonist-evoked Ca(2+) wave progression requires Ca(2+) and IP(3).
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Agonist-evoked Ca(2+) wave progression requires Ca(2+) and IP(3).

机译：Agonist-evoked Ca(2 +)波发展要求Ca(2 +)和IP(3)。

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摘要

Smooth muscle responds to IP(3)-generating agonists by producing Ca(2+) waves. Here, the mechanism of wave progression has been investigated in voltage-clamped single smooth muscle cells using localized photolysis of caged IP(3) and the caged Ca(2+) buffer diazo-2. Waves, evoked by the IP(3)-generating agonist carbachol (CCh), initiated as a uniform rise in cytoplasmic Ca(2+) concentration ([Ca(2+)](c)) over a single though substantial length (approximately 30 microm) of the cell. During regenerative propagation, the wave-front was about 1/3 the length (approximately 9 microm) of the initiation site. The wave-front progressed at a relatively constant velocity although amplitude varied through the cell; differences in sensitivity to IP(3) may explain the amplitude changes. Ca(2+) was required for IP(3)-mediated wave progression to occur. Increasing the Ca(2+) buffer capacity in a small (2 microm) region immediately in front of a CCh-evoked Ca(2+) wave halted progression at the site. However, the wave front does not progress by Ca(2+)-dependent positive feedback alone. In support, colliding [Ca(2+)](c) increases from locally released IP(3) did not annihilate but approximately doubled in amplitude. This result suggests that local IP(3)-evoked [Ca(2+)](c) increases diffused passively. Failure of local increases in IP(3) to evoke waves appears to arise from the restricted nature of the IP(3) increase. When IP(3) was elevated throughout the cell, a localized increase in Ca(2+) now propagated as a wave. Together, these results suggest that waves initiate over a surprisingly large length of the cell and that both IP(3) and Ca(2+) are required for active propagation of the wave front to occur.
机译：平滑肌对IP(3)模型受体激动剂通过生产Ca(2 +)波。波发展的机制调查在voltage-clamped单一光滑肌肉细胞使用本地化的光解的笼子里IP(3)和笼子里的Ca(2 +)缓冲diazo-2。诱发的IP(3)模型”受体激动剂氯化氨甲酰胆碱(CCh),开始作为一个统一的细胞质Ca(2 +)浓度((Ca (2 +)) (c))在一个单一的尽管大量的长度(大约30岁microm)的细胞。传播,波面约为1/3起始的长度(约9 microm)网站。恒定的速度虽然振幅变化通过细胞;IP(3)可以解释振幅的变化。需要IP(3)介导波进展吗发生。在一个小(2 microm)地区立即在前面CCh-evoked Ca(2 +)波停止发展该网站。进步的Ca(2 +)端依赖积极的反馈一个人。增加从本地IP(3)并未公布湮灭,但大约翻了一番振幅。IP(3)诱发(Ca (2 +)) (c)增加扩散被动。唤起波似乎来自限制IP的性质(3)增加。在整个细胞升高,局部Ca(2 +)现在增加传播的波。在一起,这些结果表明,波发起了一个惊人的长度细胞和IP(3)和Ca(2 +)是必需的积极传播的波前发生。

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