Mechanisms of Ca(2+)-independent contraction in single permeabilized ferret aorta cells.
Mechanisms of Ca(2+)-independent contraction in single permeabilized ferret aorta cells.
复制标题
单个透化雪貂主动脉细胞中 Ca(2 ) 独立收缩的机制。
DOI：
10.1161/01.res.72.3.651
复制
发表时间：
1993
影响因子：
20.1
通讯作者：
Morgan,KG
中科院分区：
文献类型：
--
作者：
Katsuyama,H;Morgan,KG
通过直接测量雪貂主动脉单个皂苷渗透的平滑肌细胞的力，研究了前列腺素F2 α（PGF 2 α）在细胞内Ca 2+恒定的情况下引起收缩的机制。PGF2 α收缩的大小在pCa 9.0和pCa 6.6之间没有变化。其余实验在pCa 7.0下进行。在pCa 7.0时，PGF2 α（0.1 - 100 microM）以剂量依赖性方式诱导持续力，在10分钟内达到最大值（2.61 +/-0.20 microN，n = 14）。蛋白激酶C假底物抑制剂（3 μ M）和staurosporine（1 μ M）均显著抑制PGF 2 α（100 μ M）诱导的收缩，但staurosporine更有效。星形孢菌素引起88.8 +/-13.3%的抑制，而蛋白激酶C假底物抑制剂抑制62.3 +/-9.6%的PGF 2 α诱导的收缩。1型和2A型蛋白磷酸酶的抑制剂微囊藻毒素-LR在1 μ M的浓度下诱导逐渐和持续的收缩（1.53 +/-0.21 μ N）。较低浓度的微囊藻毒素-LR（100 nM）也诱导了小但显著的收缩（0.36 +/-0.26 microN）。用1 μ M和100 nM微囊藻毒素-LR预处理可显著抑制PGF 2 α诱导的收缩，分别从2.61 +/-0.20 microN（n = 14）降至0.32 +/-0.20 microN（n = 6）（p <0.01）和1.52 +/-0.21 microN（n = 6）（p <0.01）。这些结果表明，在恒定的低细胞内Ca2+下发生的PGF 2 α诱导的收缩部分是蛋白激酶C激活和磷酸酶抑制的综合结果。
The mechanisms by which prostaglandin F2 alpha (PGF2 alpha) can cause contractions at constant intracellular Ca2+ were investigated by the direct measurement of force from single saponin-permeabilized smooth muscle cells from the ferret aorta. The size of PGF2 alpha contractions did not change between pCa 9.0 and pCa 6.6. The remainder of the experiments were carried out at pCa 7.0. At pCa 7.0, PGF2 alpha (0.1-100 microM) induced sustained force in a dose-dependent manner, reaching a maximum (2.61 +/- 0.20 microN, n = 14) in 10 minutes. Both protein kinase C pseudosubstrate inhibitor (3 microM) and staurosporine (1 microM) significantly inhibited PGF2 alpha (100 microM)-induced contractions, but staurosporine was more effective. Staurosporine caused 88.8 +/- 13.3% inhibition, whereas protein kinase C pseudosubstrate inhibitor inhibited 62.3 +/- 9.6% of the PGF2 alpha-induced contraction. An inhibitor of type-1 and type-2A protein phosphatases, microcystin-LR, at a concentration of 1 microM induced a gradual and sustained contraction (1.53 +/- 0.21 microN). A lower concentration of microcystin-LR (100 nM) also induced a small but significant contraction (0.36 +/- 0.26 microN). Pretreatment with both 1 microM and 100 nM microcystin-LR caused significant inhibition of the PGF2 alpha-induced contraction from 2.61 +/- 0.20 microN (n = 14) to 0.32 +/- 0.20 microN (n = 6) (p < 0.01) and 1.52 +/- 0.21 microN (n = 6) (p < 0.01), respectively. These results indicate that the part of the PGF2 alpha-induced contraction that occurs at a constant, low intracellular Ca2+ is the combined result of activation of protein kinase C and phosphatase inhibition.