Rasmussen H, Forder J, Kojima I, Scriabine A
Biochem Biophys Res Commun. 1984 Jul 31;122(2):776-84. doi: 10.1016/s0006-291x(84)80101-1.
Myosin light chain phosphorylation may not regulate the sustained phase of vascular smooth muscle contraction. Another, unidentified, calcium-dependent pathway may be involved in this process. TPA, an activator of C-kinase, at concentrations of 10 to 333 nM induces a calcium-dependent contraction of vascular smooth muscle which develops slowly but progressively to reach values of 50-300 mm Hg. Arteries exposed to the ionophore A23187, in a calcium-free medium, display a uniform series of contractile responses when exposed to 1.5 mM Ca2+ for 2 min once every 10 min. Exposure to 100 nM TPA as well as ionophore leads to a progressive enhancement of these calcium-induced, contractile responses. Arteries stimulated by brief (10 sec), repetitive (every 3 min) electrical pulses, respond with a series of comparable phase 1 responses. Prior exposure of vessels to 10 nM TPA, causes a progressive increase in the magnitude of these responses to repetitive electrical stimulation. Addition of 25 microM forskolin, an activator of adenylate cyclase, to TPA-treated, partially-contracted muscle leads to the immediate inhibition of the TPA-induced contraction. These data suggest that the activation of C-kinase plays a significant role in regulating vascular smooth muscle contraction.
肌球蛋白轻链磷酸化可能并不调节血管平滑肌收缩的持续阶段。可能存在另一条未明确的、依赖钙的途径参与这一过程。佛波酯（TPA），一种蛋白激酶C的激活剂，浓度在10至333纳摩尔时可诱导血管平滑肌产生依赖钙的收缩，这种收缩发展缓慢但持续增强，可达50 - 300毫米汞柱。在无钙培养基中用离子载体A23187处理的动脉，每10分钟暴露于1.5毫摩尔钙离子中2分钟时，会呈现出一系列均匀的收缩反应。暴露于100纳摩尔TPA以及离子载体都会导致这些钙诱导的收缩反应逐渐增强。用短暂（10秒）、重复（每3分钟一次）的电脉冲刺激动脉，会产生一系列类似的第一阶段反应。预先将血管暴露于10纳摩尔TPA，会使这些对重复电刺激的反应幅度逐渐增加。向经TPA处理的部分收缩的肌肉中添加25微摩尔的福斯可林（一种腺苷酸环化酶激活剂），会立即抑制TPA诱导的收缩。这些数据表明蛋白激酶C的激活在调节血管平滑肌收缩中起重要作用。
