Moreland S, Moreland R S
Am J Physiol. 1987 Jun;252(6 Pt 2):H1049-58. doi: 10.1152/ajpheart.1987.252.6.H1049.
Contraction of swine carotid medial fibers with KCl results in stress development associated with high levels of myosin light chain (MLC) phosphorylation and maximum shortening velocity (V0) indicative of rapidly cycling phosphorylated cross bridges. The period of stress maintenance is characterized by low levels of MLC phosphorylation and V0; the maintained stress is postulated to be supported by dephosphorylated, slowly cycling cross bridges (latch bridges). This study was designed to examine the roles of calcium in both stress development and stress maintenance. Medial strips were contracted with 110 mM KCl in the presence of varying concentrations of the calcium channel blocker nifedipine (1-100 nM) or were contracted with varying concentrations of the calcium channel activator BAY-K 8644 (0.3-3 microM). Nifedipine significantly depressed stress maintenance and V0, but had little effect on either stress development or MLC phosphorylation. Conversely, BAY-K 8644 produced contractions that were equal to those elicited with 110 mM KCl but that were characterized by low levels of V0 and basal or low levels of MLC phosphorylation. These data suggest that the mechanisms by which the cellular calcium concentration increases and the limitations on this increase may impact differently on different regulatory processes of contraction and, thereby, on cross bridge behavior.
用氯化钾使猪颈动脉内侧纤维收缩会导致应力产生，同时伴有高水平的肌球蛋白轻链（MLC）磷酸化和最大缩短速度（V0），这表明磷酸化横桥快速循环。应力维持阶段的特征是MLC磷酸化水平和V0较低；据推测，维持的应力由去磷酸化的、缓慢循环的横桥（闭锁桥）支持。本研究旨在探讨钙在应力产生和应力维持中的作用。在存在不同浓度的钙通道阻滞剂硝苯地平（1 - 100 nM）的情况下，用110 mM氯化钾使内侧条带收缩，或者用不同浓度的钙通道激活剂BAY - K 8644（0.3 - 3 microM）使内侧条带收缩。硝苯地平显著降低应力维持和V0，但对应力产生或MLC磷酸化影响很小。相反，BAY - K 8644产生的收缩与用110 mM氯化钾引起的收缩相同，但特征是V0水平较低以及MLC磷酸化处于基础水平或较低水平。这些数据表明，细胞钙浓度增加的机制及其增加的限制可能对收缩的不同调节过程产生不同影响，从而对横桥行为产生不同影响。
