Contributions of intracellular and extracellular Ca2+ pools to activation of myosin phosphorylation and stress in swine carotid media.
Contributions of intracellular and extracellular Ca2+ pools to activation of myosin phosphorylation and stress in swine carotid media.
复制标题
细胞内和细胞外 Ca2 库对猪颈动脉中肌球蛋白磷酸化和应激激活的贡献。
DOI：
10.1161/01.res.60.3.410
复制
发表时间：
1987
影响因子：
20.1
通讯作者：
Murphy,RA
中科院分区：
文献类型：
--
作者：
Ratz,PH;Murphy,RA
收缩激动剂可以动员Ca2+从细胞内和细胞外储存在平滑肌。这项研究解决了Ca2+动员的作用，因为它涉及到Ca2+调节平滑肌收缩系统的复杂方式。在猪颈动脉介质中，组胺和苯肾上腺素都产生肌球蛋白磷酸化和应激的初始快速增加。应激在刺激持续期间持续，而肌球蛋白磷酸化缓慢下降到稳态水平。去除细胞外Ca2+或消除细胞Ca2+内流并没有显著降低由两种激动剂产生的肌球蛋白磷酸化的初始快速增加，但将肌球蛋白磷酸化的稳态水平降低到基础值。最初的压力迅速增加，但压力并没有维持下去。在肌浆网Ca2+耗竭后，在苯肾上腺素存在的情况下，Ca2+内流引起的肌肉激活在肌球蛋白磷酸化中没有最初的短暂性，并且应激发展缓慢。肌球蛋白磷酸化和应激的稳态水平与控制值没有差异。组胺也得到了类似的结果，尽管肌球蛋白的短暂磷酸化也被观察到。这些结果与假设一致，即肌浆网在血管平滑肌中的作用是提供高肌浆Ca2+浓度，引起广泛的肌球蛋白磷酸化和快速的过桥循环，导致快速的应激发展。在细胞外Ca2+存在的情况下，当细胞内Ca2+池被耗尽时，激动剂诱导的稳态应激和肌球蛋白磷酸化的控制水平可以在没有初始磷酸化瞬间的情况下产生，这表明肌浆网不需要在“闩锁”期间调节稳态肌浆[Ca2+]。
Contractile agonists can mobilize Ca2+ from both intracellular and extracellular stores in smooth muscle. This study addresses the role of Ca2+ mobilization as it relates to the complex manner by which Ca2+ regulates the contractile system in smooth muscle. In swine carotid media, both histamine and phenylephrine produced initial rapid increases in myosin phosphorylation and stress. Stress was sustained for the duration of the stimulus while myosin phosphorylation slowly declined to steady-state levels. Removal of extracellular Ca2+ or elimination of cellular Ca2+ influx did not dramatically reduce the initial rapid increase in myosin phosphorylation produced by either agonist but reduced steady-state levels of myosin phosphorylation to basal values. Initial rapid increases in stress were seen, but stress was not maintained. Following depletion of Ca2+ from sarcoplasmic reticulum, muscle activation by Ca2+ influx in the presence of phenylephrine occurred without an initial transient in myosin phosphorylation, and stress developed slowly. Steady-state levels of myosin phosphorylation and stress were not different from control values. Similar results were obtained with histamine, although a small transient in myosin phosphorylation was also seen. These results are consistent with the hypothesis that the role of the sarcoplasmic reticulum in vascular smooth muscle is to provide high myoplasmic Ca2+ concentrations causing extensive myosin phosphorylation and rapid crossbridge cycling leading to rapid stress development. In the presence of extracellular Ca2+, control levels of agonist-induced steady-state stress and myosin phosphorylation could be produced without an initial phosphorylation transient when intracellular Ca2+ pools were depleted, suggesting that the sarcoplasmic reticulum is not required for the regulation of steady-state myoplasmic [Ca2+] during "latch".
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DOI：
--
发表时间：
1985
期刊：
影响因子：
--
作者：
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DOI：
--
发表时间：
1983
期刊：
Journal of Physiology
影响因子：
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作者：
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DOI：
--
发表时间：
1969
期刊：
Archives Internationales de Physiologie et de Biochimie
影响因子：
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作者：
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通讯作者：
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影响因子：
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作者：
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