TPA-INDUCED CONTRACTION OF ISOLATED RABBIT VASCULAR SMOOTH-MUSCLE
TPA-INDUCED CONTRACTION OF ISOLATED RABBIT VASCULAR SMOOTH-MUSCLE
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DOI：
10.1016/s0006-291x(84)80101-1
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发表时间：
1984-01-01
影响因子：
3.1
通讯作者：
SCRIABINE, A
中科院分区：
文献类型：
--
作者：
RASMUSSEN, H;FORDER, J;SCRIABINE, A
肌球蛋白轻链磷酸化可能不调节血管平滑肌收缩的持续期。另一种未知的钙依赖途径可能参与了这一过程。TPA [12-0- tetradecanoylpholl -13-acetate]是c激酶的一种活化剂，浓度为10-333 nM时，可诱导血管平滑肌的钙依赖性收缩，收缩缓慢但逐渐达到50-300毫米汞柱。在无ca的培养基中，暴露于离子载体A23187[钙霉素]的动脉，在暴露于1.5 mm Ca2+ 2分钟或每10分钟时，显示出一系列均匀的收缩反应。暴露于100nm TPA和离子载体导致这些钙诱导的收缩反应的逐步增强。动脉受到短暂的（10秒）、重复的（每3分钟）电脉冲刺激，产生一系列可比较的第一阶段反应。先前暴露于10 nM TPA的血管，会导致这些对重复电刺激的反应幅度逐渐增加。新增25亩。一种腺苷酸环化酶的激活剂M forskolin，对tpa处理的，部分收缩的肌肉导致tpa诱导的收缩的立即抑制。c激酶的激活可能在调节血管平滑肌收缩中起重要作用。
Myosin light chain phosphorylation may not regulate the sustained phase of vascular smooth muscle contraction. Another, unidentified, Ca-dependent pathway may be involved in this process. TPA [12-0-tetradecanoylphorbol-13-acetate], an activator of C-kinase, at concentrations of 10-333 nM induces a Ca-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 [calcimycin], in a Ca-free medium, display a uniform series of contractile responses when exposed to 1.5 mM Ca2+ for 2 min onve every 10 min. Exposure to 100 nM TPA as well as ionophore leads to a progressive enhancement of these Ca-induced, contractile responses. Arteries stimulated by brief (10 s), 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 .mu.M forskolin, an activator of adenylate cyclase, to TPA-treated, partially-contracted muscle leads to the immediate inhibition of the TPA-induced contraction. The activation of C-kinase may play a significant role in regulating vascular smooth muscle contraction.