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Study for the calcium extrusion mechanism in pregnant human myometrium.

妊娠人子宫肌层钙排出机制的研究。

基本信息

批准号：
06671698
负责人：
KAWARABAYASHI Tatsuhiko
金额：
$ 1.28万
依托单位：
Fukuoka University
依托单位国家：
日本
项目类别：
Grant-in-Aid for Scientific Research (C)
财政年份：
1994
资助国家：
日本
起止时间：
1994 至 1996
项目状态：
已结题

项目摘要

Periodic uterine relaxation in labor relieves the fetus from hypoxia related to sustained contractions. A reduction in intracellular calcium is essential for relaxation. Therefore we aimed to clarify the extrusion mechanisms of intracellular calcium ions in pregnant human myometrium.Isometric contraction of small muscle bundles obtained from human myometrium at term was recorded. High-potassium and sodium-free solutions could induce stable contractures that revealed initial phasic contractions followed by tonic contractions. The effects of external calcium, external magnesium, nifedipine, and calcium-ATPase inhibitors on both contractures were then examined.Because maximum tonic contraction was induced by 48 mM potassium, this concentration was used. Both contractures depended on external calcium concentrations. Nifedipine, 10^<-7>M inhibited both initial phasic contractions and the tonic phase of the high-potassium contracture ; however, it could not suppress the tonic phase of the sodium-free contracture. Calcium-ATPase inhibitors, cyclopiazonic acid and lauryl sulfate, potentiated the tensions of tonic phases in both contractures ; the effect of lauryl sulfate was stronger than that of cyclopiazonic acid.When external magnesium was gradually increased from 0 to 9.6 mM,both phasic contractions and the tonic phase of the high-potassium contracture transiently increased, followed by a reduction of tension, whereas the tonic phase of the sodium-free contracture was markedly inhibited by magnesium in a dose-dependent manner.These results suggest that the presence of the sodium-calcium exchange mechanism and the specific inhibitory effect of magnesium were indicated in human myometrium during pregnancy. These mechanisms might prevent the long tonic contractions, to protect the fetus from hypoxia during pregnancy and parturition.

产程中周期性的子宫舒张可使胎儿从持续性宫缩引起的缺氧中解脱出来。细胞内钙离子的减少对放松是必不可少的。因此，我们的目的是阐明细胞内钙离子在妊娠人子宫肌层的挤出机制。高钾和无钠溶液可诱导稳定的挛缩，表现为初始阶段性收缩，随后为强直性收缩。然后检查了外源性钙、外源性镁、硝苯地平和钙-ATP酶抑制剂对两种挛缩的影响，因为48 mM钾可诱导最大强直性收缩，所以使用该浓度。这两种挛缩都依赖于外部钙浓度。硝苯地平，10 μ <-7>M抑制初始阶段的收缩和紧张阶段的高钾挛缩，但是，它不能抑制紧张阶段的无钠挛缩。钙-ATP酶抑制剂环匹阿尼酸和十二烷基硫酸盐可增强两种挛缩的张力相张力;当外部镁从0逐渐增加到9.6mM时，高钾挛缩的时相收缩和强直相都短暂增加，随后张力降低，而无钠收缩的强直相则被镁以剂量依赖的方式显著抑制，这些结果表明，妊娠期人子宫肌层存在钠钙交换机制，镁具有特异性抑制作用。这些机制可能阻止长时间的紧张性收缩，以保护胎儿在妊娠和分娩期间免受缺氧。