RELAXATION OF ARTERIAL SMOOTH-MUSCLE BY CALCIUM SPARKS
RELAXATION OF ARTERIAL SMOOTH-MUSCLE BY CALCIUM SPARKS
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DOI：
10.1126/science.270.5236.633
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发表时间：
1995-10-27
期刊：
影响因子：
56.9
通讯作者：
LEDERER, WJ
中科院分区：
文献类型：
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作者：
NELSON, MT;CHENG, H;LEDERER, WJ
平滑肌肌浆网（SR）中兰尼碱敏感的钙释放通道激活导致细胞内钙离子浓度（[Ca²⁺]ᵢ）局部升高，从而引起动脉扩张。在肌源性脑动脉的单个平滑肌细胞的表面膜下观察到来自肌浆网的[Ca²⁺]ᵢ的兰尼碱敏感的自发性局部升高（Ca²⁺火花）。兰尼碱和毒胡萝卜素抑制Ca²⁺火花以及钙依赖性钾（K - Ca）电流，这表明Ca²⁺火花激活K - Ca通道。此外，由Ca²⁺火花激活的K - Ca通道似乎使加压的肌源性动脉超极化并扩张，因为兰尼碱和毒胡萝卜素使这些动脉去极化和收缩的程度与K - Ca通道阻滞剂所产生的程度相似。Ca²⁺火花通过激活K - Ca通道间接引起血管舒张，但对调节收缩的空间平均[Ca²⁺]ᵢ几乎没有直接影响。
Local increases in intracellular calcium ion concentration ([Ca2+](i)) resulting from activation of the ryanodine-sensitive calcium-release channel in the sarcoplasmic reticulum (SR) of smooth muscle cause arterial dilation. Ryanodine-sensitive, spontaneous local increases in [Ca2+](i) (Ca2+ sparks) from the SR were observed just under the surface membrane of single smooth muscle cells from myogenic cerebral arteries. Ryanodine and thapsigargin inhibited Ca2+ sparks and Ca2+-dependent potassium (K-Ca), currents, suggesting that Ca2+ sparks activate K-Ca channels. Furthermore, K-Ca channels activated by Ca2+ sparks appeared to hyperpolarize and dilate pressurized myogenic arteries because ryanodine and thapsigargin depolarized and constricted these arteries to an extent similar to that produced by blockers of K-Ca channels. Ca2+ sparks indirectly cause vasodilation through activation of K-Ca channels, but have little direct effect on spatially averaged [Ca2+](i), which regulates contraction.