Chang Katherine
Center for Perinatal Biology, Department of Physiology and Pharmacology, Loma Linda University School of Medicine, Loma Linda, California 62350, USA.
Reprod Sci. 2008 Apr;15(4):336-48. doi: 10.1177/1933719108317975.
Pregnancy is a physiological state that involves a significant decrease in uterine vascular tone and an increase in uterine blood flow, which is mediated in part by steroid hormones, including estrogen, progesterone, and cortisol. Previous studies have demonstrated the involvement of these hormones in the regulation of uterine artery contractility through signaling pathways specific to the endothelium and the vascular smooth muscle. Alterations in endothelial nitric oxide synthase expression and activity, nitric oxide production, and expression of enzymes involved in PGI(2) production contribute to the uterine artery endothelium-specific responses. Steroid hormones also have an effect on calcium-activated potassium channel activity, PKC signaling pathway and myogenic tone, and alterations in pharmacomechanical coupling in the uterine artery smooth muscle. This review addresses current understanding of the molecular mechanisms by which steroid hormones including estrogen, progesterone, and cortisol modulate uterine artery contractility to alter uterine blood flow during pregnancy with an emphasis on the pregnant ewe model.
怀孕是一种生理状态,涉及子宫血管张力显著降低和子宫血流量增加,这部分是由类固醇激素介导的,包括雌激素、孕酮和皮质醇。先前的研究表明,这些激素通过内皮细胞和血管平滑肌特有的信号通路参与子宫动脉收缩性的调节。内皮型一氧化氮合酶表达和活性、一氧化氮生成以及参与前列环素(PGI₂)生成的酶的表达改变,促成了子宫动脉内皮特异性反应。类固醇激素还对钙激活钾通道活性、蛋白激酶C信号通路和肌源性张力有影响,以及子宫动脉平滑肌中药力机械偶联的改变。本综述阐述了目前对包括雌激素、孕酮和皮质醇在内的类固醇激素调节子宫动脉收缩性以改变孕期子宫血流量的分子机制的理解,重点是怀孕母羊模型。