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首页> 外文期刊>American Journal of Physiology >Adaptation of uterine artery thick- and thin-filament regulatory pathways to pregnancy.
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Adaptation of uterine artery thick- and thin-filament regulatory pathways to pregnancy.

机译：子宫动脉粗细丝调节途径对妊娠的适应。

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摘要

Little is known about the adaptation of uterine artery smooth muscle contractile mechanisms to pregnancy. The present study tested the hypothesis that pregnancy differentially regulates thick- and thin-filament regulatory pathways in uterine arteries. Isometric tension, intracellular free Ca(2+) concentration, and phosphorylation of 20-kDa myosin light chain (MLC(20)) were measured simultaneously in uterine arteries isolated from nonpregnant and near-term (140 days gestation) pregnant sheep. Phenylephrine-mediated intracellular free Ca(2+) concentration, MLC(20) phosphorylation, and contraction tension were significantly increased in uterine arteries of pregnant compared with nonpregnant animals. In contrast, phenylephrine-mediated Ca(2+) sensitivity of MLC(20) phosphorylation was decreased in the uterine arteries of pregnant sheep. Simultaneous measurement of phenylephrine-stimulated tension and MLC(20) phosphorylation in the same tissue indicated a decrease in MLC(20) phosphorylation-independent contractions in the uterine arteries of pregnant sheep. In addition, activation of PKC produced significantly lower sustained contractions in uterine arteries of pregnant compared with nonpregnant animals in the absence of changes in MLC(20) phosphorylation levels in either vessels. In uterine arteries of nonpregnant sheep, the mitogen-activated protein kinase kinase/extracellular signal-regulated kinase inhibitor PD-098059 significantly increased phenylephrine-mediated, MLC(20) phosphorylation-independent contractions. The results suggest that in uterine arteries, pregnancy upregulates alpha(1)-adrenoceptor-mediated Ca(2+) mobilization and MLC(20) phosphorylation. In contrast, pregnancy downregulates the Ca(2+) sensitivity of myofilaments, which is mediated by both thick- and thin-filament pathways.
机译：关于子宫动脉平滑肌收缩机制适应妊娠的知之甚少。本研究检验了妊娠差异调节子宫动脉中的粗丝和细丝调节途径的假说。等轴测张力，细胞内游离Ca（2+）浓度和20 kDa肌球蛋白轻链（MLC（20））的磷酸化同时测量从未怀孕和近期（妊娠140天）怀孕的绵羊分离的子宫动脉。苯肾上腺素介导的细胞内游离Ca（2+）浓度，MLC（20）磷酸化和收缩张力在怀孕的子宫动脉中与未怀孕的动物相比明显增加。相比之下，苯肾上腺素介导的MLC（20）磷酸化的Ca（2+）敏感性在孕妇绵羊的子宫动脉中降低。苯肾上腺素刺激的紧张度和MLC（20）磷酸化在同一组织中的同时测量表明孕绵羊子宫动脉MLC（20）磷酸化非依赖性收缩减少。此外，与未怀孕的动物相比，在任一血管中MLC（20）磷酸化水平均没有变化的情况下，PKC的激活在孕妇的子宫动脉中产生的持续收缩明显降低。在非妊娠绵羊的子宫动脉中，促分裂原激活的蛋白激酶激酶/细胞外信号调节激酶抑制剂PD-098059显着增加了去氧肾上腺素介导的MLC（20）磷酸化依赖性收缩。结果表明，在子宫动脉中，妊娠上调α（1）-肾上腺素受体介导的Ca（2+）动员和MLC（20）磷酸化。相比之下，怀孕下调了由细丝和细丝途径介导的肌丝Ca（2+）敏感性。

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