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首页> 外文期刊>American Journal of Physiology >Different roles of ryanodine receptors and inositol (1,4,5)-trisphosphate receptors in adrenergically stimulated contractions of small arteries.
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Different roles of ryanodine receptors and inositol (1,4,5)-trisphosphate receptors in adrenergically stimulated contractions of small arteries.

机译：肾上腺素刺激小动脉收缩中，ryanodine受体和肌醇（1,4,5）-三磷酸受体的不同作用。

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摘要

The functions of ryanodine receptors (RyRs) and inositol (1,4,5)-trisphosphate receptors [Ins(1,4,5)P(3)Rs] in adrenergically activated contractions of pressurized rat mesenteric small arteries were investigated. Caffeine (20 mM) but not phenylephrine (PE; 10 microM) facilitated the depletion of smooth muscle sarcoplasmic reticulum (SR) Ca(2+) stores by ryanodine (40 microM). In ryanodine-treated SR-depleted arteries, 1) Ca(2+) sparks were absent, 2) low concentrations of PE failed to elicit either vasoconstriction or normal asynchronous propagating Ca(2+) waves, and 3) high [PE] induced abnormally slow oscillatory contractions (vasomotion) and synchronous Ca(2+) oscillations. In ryanodine-treated SR-depleted arteries denuded of endothelium, high [PE] induced steady contraction and steady elevation of intracellular [Ca(2+)]. In contrast, 2-aminoethyl diphenylborate (2-APB), a putative blocker of Ins(1,4,5)P(3)Rs, produced opposite effects to ryanodine: 1) Ca(2+) sparks were present; 2) Ca(2+) waves were absent; 3) caffeine-releasable Ca(2+) stores were intact; and 4) PE, even at high concentrations on endothelial-denuded arteries, failed to elicit contraction, asynchronous Ca(2+) waves, or synchronous Ca(2+) oscillations or maintained elevated [Ca(2+)]. We conclude that 1) Ins(1,4,5)P(3)Rs are essential for adrenergically induced asynchronous Ca(2+) waves and the associated steady vasoconstriction, 2) RyRs are not appreciably opened during adrenergic activation (because PE did not facilitate the development of the effects of ryanodine), and 3) Ins(1,4,5)P(3)Rs are not essential for Ca(2+) sparks. This provides an explanation of the fact that adrenergic stimulation decreases the frequency of Ca(2+) sparks (previously reported) while simultaneously increasing the frequency of asynchronous propagating Ca(2+) waves; different SR Ca(2+)-release channels are involved.
机译：ryanodine受体（RyRs）和肌醇（1,4,5）-三磷酸受体[Ins（1,4,5）P（3）Rs]在加压大鼠肠系膜小动脉的肾上腺素能激活的收缩中的功能进行了研究。咖啡因（20 mM），而不是去氧肾上腺素（PE; 10 microM）促进了赖诺丹（40 microM）消耗的平滑肌肌质网（SR）Ca（2+）存储。在用ryanodine处理的SR衰竭的动脉中，没有1）Ca（2+）火花，2）低浓度的PE无法引起血管收缩或正常的异步传播Ca（2+）波，以及3）高[PE]诱导异常缓慢的振荡收缩（血管运动）和同步Ca（2+）振荡。在莱丹定治疗的内皮剥夺的SR耗尽动脉中，高[PE]引起稳定的收缩和细胞内[Ca（2+）]的稳定升高。相反，Ins（1,4,5）P（3）Rs的公认阻滞剂2-氨基乙基二苯硼酸酯（2-APB）与ryanodine产生相反的作用：1）存在Ca（2+）火花; 2）缺少Ca（2+）波; 3）咖啡因可释放的Ca（2+）存储完整。和4）PE，即使在内皮剥夺的动脉上浓度很高，也未能引起收缩，异步Ca（2+）波或同步Ca（2+）振荡或维持升高的[Ca（2+）]。我们得出以下结论：1）Ins（1,4,5）P（3）Rs对于肾上腺素能诱导的异步Ca（2+）波和相关的稳定血管收缩是必不可少的，2）RyRs在肾上腺素能激活期间未明显打开（因为PE确实如此）不能促进ryanodine效应的发展），以及3）Ins（1,4,5）P（3）Rs对于Ca（2+）火花不是必不可少的。这提供了以下事实的解释：肾上腺素能刺激降低了Ca（2+）火花的频率（先前已报道），同时增加了异步传播的Ca（2+）波的频率;不同的SR Ca（2 +）-释放通道涉及。

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