Oxytocin-induced phasic and tonic contractions are modulated by the contractile machinery rather than the quantity of oxytocin receptor
Oxytocin-induced phasic and tonic contractions are modulated by the contractile machinery rather than the quantity of oxytocin receptor
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DOI：
10.1152/ajpendo.00492.2006
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发表时间：
2007-04-01
影响因子：
5.1
通讯作者：
Nishimori, Katsuhiko
中科院分区：
文献类型：
--
作者：
Kawamata, Masaki;Tonomura, Yutaka;Nishimori, Katsuhiko
催产素诱导的阶段性和强直性收缩是由收缩机制而不是催产素受体的数量调节的。 Am J Physiol Endocrinol Metab 292：E992-E999，2007。首次发表于 2006 年 12 月 5 日； doi：10.1152/ajpendo.00492.2006。 - 为了系统地研究催产素（OT）受体（OTR）数量与收缩特征之间的关系，我们测量了OTR和L型Ca2+通道α（1C）亚基（α（1C））的mRNA表达水平，并检查了OT诱导的小鼠子宫纵向平滑肌的阶段性或强直性收缩的调节机制。 19.0 G（妊娠19.0 d）OTR mRNA 表达量高于非妊娠期，发情期和19.0 G α(1C) mRNA 表达量高于动情间期。 OT 引起的宫缩在发情间期很少发生。在发情期和 19.0 G 期间，维拉帕米消除了低浓度 OT 诱导的全型或无型阶段性收缩。OT 诱导的强直性收缩在发情期和 19.0 G 中具有相似的 pD(2) 值。然而，19.0 G 时的幅度远大于动情期。尽管 OTR 量较小，但 PGF(2α) 受体 (FP) 敲除小鼠在 19.0 G 时也出现了较大的强直性收缩。 Verapamil 和 Y-27632 部分抑制 19.0 G 时的强直收缩。在 19.0 G 时，环匹阿尼酸诱导的强直收缩随着 OT 诱导的强直收缩的增加而相应减少。这些结果表明，阶段性收缩依赖于 α(1C)。 19.0 G 的强直收缩依赖于通过 L 型 Ca2+ 通道和钙库操纵的 Ca2+ 通道的 Ca2+ 流入，并且力通过 Rho 信号通路增强，从而增加了 Ca2+ 敏感性。因此，子宫收缩主要是通过收缩信号机制的改变来控制的，而不是简单地通过OTR的量来控制。
Oxytocin-induced phasic and tonic contractions are modulated by the contractile machinery rather than the quantity of oxytocin receptor. Am J Physiol Endocrinol Metab 292: E992-E999, 2007. First published December 5, 2006; doi:10.1152/ajpendo.00492.2006. - To investigate the relationship between the oxytocin (OT) receptor (OTR) quantity and the contractile features systematically, we measured the mRNA expression levels of OTR and L-type Ca2+ channel alpha(1C)-subunit (alpha(1C)) and examined the regulatory mechanisms of OT-induced phasic or tonic contractions of the longitudinal smooth muscles in mouse uteri. The mRNA expression of OTR in 19.0 G (19.0 days of gestation) was greater than those in nonpregnant phases, and that of alpha(1C) in estrus and 19.0 G was higher than in diestrus. OT-induced contractions sparsely occurred in diestrus. The OT-induced all-or-none-type phasic contractions at low concentrations were abolished by verapamil in both estrus and 19.0 G. OT-induced tonic contractions had similar pD(2) values in both estrus and 19.0 G. However, the magnitude in 19.0 G was much greater than that in estrus. The large tonic contractions also occurred in PGF(2 alpha) receptor ( FP) knockout mice in 19.0 G despite a small amount of OTR. Verapamil and Y-27632 partially inhibited the tonic contractions in 19.0 G. Cyclopiazonic acid-induced tonic contractions were reciprocally decreased with the increase in the OT-induced ones in 19.0 G. These results indicate that the phasic contractions are dependent on alpha(1C). The tonic contractions in 19.0 G are dependent on both Ca2+ influxes via L-type Ca2+ channels and store-operated Ca2+ channels, and the force is augmented by the Rho signal pathway, which increases the Ca2+ sensitivity. Thus the uterine contractions are mainly controlled by the modification of contractile signal machinery rather than simply by the OTR quantity.