首页> 外文期刊>FEBS Letters >Basic properties of a novel ryanodine‐sensitive, caffeine‐insensitive calcium‐induced calcium release mechanism in permeabilised human vascular smooth muscle cells
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Basic properties of a novel ryanodine‐sensitive, caffeine‐insensitive calcium‐induced calcium release mechanism in permeabilised human vascular smooth muscle cells

机译:新颖的对精氨酸,咖啡因不敏感的钙诱导的人血管平滑肌细胞钙释放机制的基本特性

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>The efflux of 45Ca2+ from preloaded intracellular stores of saponin-permeabilised human uterine artery smooth muscle cultured cells was used to study the mechanisms underlying Ca2+ release from the sarcoplasmic reticulum (SR). The present paper demonstrates directly a functional Ca2+ release mechanism that is dependent on an increase in free Ca2+ (100 nM-30 μM) and is completely inhibited by 20 μM Ruthenium red. The amount of Ca2+ released at 30 μM free Ca2+ was reduced by approximately 50% compared to the release at 10 μM. This Ca2+-induced Ca2+ release (CICR) mechanism was not sensitive to caffeine. Exposure of cells to low free Ca2+-containing solutions (10 nM) indicated that a component of the CICR mechanism may be functional at basal free Ca2+ levels of 100 nM. Application of ryanodine (0.1–100 μM) induced 45Ca2+ efflux from the sarcoplasmic reticulum and this release was also inhibited by 20 μM Ruthenium red.
机译:>使用预先装载的皂素透化的人子宫动脉平滑肌细胞的细胞内 45 Ca 2 + 外排,研究Ca 的潜在机制从肌浆网(SR)释放2 + 。本文直接证明了功能性Ca 2 + 释放机制,该机制取决于游离Ca 2 + (100 nM-30μM)的增加,并被20 μM钌红。与10μM的释放相比,在30μM的游离Ca 2 + 释放的Ca 2 + 的量减少了大约50%。 Ca 2 + 诱导的Ca 2 + 释放(CICR)机制对咖啡因不敏感。将细胞暴露于低游离Ca 2 + 溶液(10 nM)中表明,CICR机制的某个组分可能在100的基础游离Ca 2 + 水平上起作用nM。施用莱丹定(0.1–100μM)可诱导肌浆网中的 45 Ca 2 + 外排,并且这种释放也被20μM钌红抑制。

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