Temporal aspects of Ca(2+) and myosin phosphorylation during myogenic and norepinephrine-induced arteriolar constriction.
Temporal aspects of Ca(2+) and myosin phosphorylation during myogenic and norepinephrine-induced arteriolar constriction.
复制标题
肌源性和去甲肾上腺素诱导的小动脉收缩期间 Ca(2 ) 和肌球蛋白磷酸化的时间方面。
DOI：
10.1159/000054089
复制
发表时间：
2000
影响因子：
1.7
通讯作者：
Hill,MA
中科院分区：
文献类型：
--
作者：
Zou,H;Ratz,PH;Hill,MA
先前的研究表明，维持稳态肌张力需要ca2 +依赖性肌球蛋白磷酸化。目前的研究通过检测在急性腔内压力和去甲肾上腺素刺激下ca2 +、肌球蛋白磷酸化和血管直径之间的时间关系进一步证实了这些观察结果。大鼠胸肌小动脉插管，并加载ca2 +敏感指示剂fura-2。用二维凝胶电泳法测定肌球蛋白磷酸化程度。腔内压力的急性升高引起细胞内ca2 +([ca2 +] i)的双相增加，其特征是短暂的峰值，然后下降到稳态水平，该水平仍然明显高于对照组。峰值[ca2 +] i与血管扩张显著相关，随血管壁张力的变化而升高。增加的腔内压力导致肌球蛋白磷酸化的单相增加，这与瞬时壁张力显著相关。一般来说，去甲肾上腺素诱导了更大的[ca2 +] i瞬态和双相肌球蛋白磷酸化模式。结果表明：(a) ca2 +和肌球蛋白磷酸化在小动脉肌生成和去甲肾上腺素诱导的反应中起主要作用；(b)在肌生成反应中ca2 +和磷酸化的变化与壁张力的变化有关，(c)两种收缩模式之间ca2 +和磷酸化模式的差异反映了潜在信号机制的可能差异。这些数据进一步强调，自发小动脉张力代表了一种维持平滑肌激活的状态，这种状态需要增加[ca2 +] i和肌球蛋白轻链磷酸化。
Previous studies demonstrated that maintenance of steady-state myogenic tone requires Ca 2+-dependent myosin phosphorylation. The present studies furthered these observations by examining temporal relationships among Ca 2+, myosin phosphorylation and vessel diameter during acute increases in intraluminal pressure and norepinephrine stimulation. Rat cremaster muscle arterioles were cannulated and loaded with the Ca 2+-sensitive indicator fura-2. The extent of myosin phosphorylation was measured using two-dimensional gel electrophoresis. Acute increases in intraluminal pressure caused a biphasic increase in intracellular Ca 2+([Ca 2+] i), characterized by a transient peak followed by a decline to a steady-state level which remained significantly higher than control values. Peak [Ca 2+] i was significantly related to vessel distension and increased with the change in wall tension. Increased intraluminal pressure resulted in a monophasic increase in myosin phosphorylation that was significantly correlated with instantaneous wall tension. In general, norepinephrine induced larger [Ca 2+] i transients and a biphasic myosin phosphorylation pattern. The results demonstrate:(a) major roles for Ca 2+ and myosin phosphorylation in arteriolar myogenic and norepinephrine-induced responses;(b) that changes in Ca 2+ and phosphorylation during a myogenic response are related to changes in wall tension, and (c) differences in Ca 2+ and phosphorylation patterns between the two modes of contraction reflect possible differences in underlying signaling mechanisms. The data further emphasize that spontaneous arteriolar tone represents a state of maintained smooth muscle activation that requires increases in [Ca 2+] i and myosin light-chain phosphorylation.