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松弛素上调小鼠子宫中的一氧化氮生物合成途径:参与抑制子宫肌层收缩。

Relaxin up-regulates the nitric oxide biosynthetic pathway in the mouse uterus: involvement in the inhibition of myometrial contractility.

作者信息

Bani D, Baccari M C, Nistri S, Calamai F, Bigazzi M, Sacchi T B

机构信息

Department of Anatomy, Histology and Forensic Medicine, University of Florence, Italy.

出版信息

Endocrinology. 1999 Oct;140(10):4434-41. doi: 10.1210/endo.140.10.7055.

DOI:10.1210/endo.140.10.7055
PMID:10499496
Abstract

The uterus is a site of nitric oxide (NO) production and expresses NO synthases (NOS), which are up-regulated during pregnancy. NO induces uterine quiescence, which is deemed necessary for the maintenance of pregnancy. Relaxin is known to promote uterine quiescence. Relaxin has also been shown to stimulate NO production in several targets. In this study we investigated the effects of relaxin on the NO biosynthetic pathway of the mouse uterus. Estrogenized mice were treated with relaxin (2 microg) for 18 h, and the uterine horns were used for determination of immunoreactive endothelial-type NOS and inducible NOS. Moreover, uterine strips from estrogenized mice were placed in an organ bath, and the effect of relaxin on K+-induced contracture was evaluated in the presence or absence of the NOS inhibitor nitro-L-arginine. Relaxin increases the expression of endothelial-type NOS in surface epithelium, glands, endometrial stromal cells, and myometrium, leaving inducible NOS expression unaffected. Moreover, relaxin inhibits myometrial contractility, and this effect is blunted by nitro-L-arginine, thus indicating that the L-arginine-NO pathway is involved in the relaxant action of relaxin on the myometrium. Because relaxin is elevated during pregnancy, it is suggested that relaxin has a physiological role in the up-regulation of uterine NO biosynthesis during pregnancy.

摘要

子宫是一氧化氮(NO)的产生部位,并表达一氧化氮合酶(NOS),这些在怀孕期间会上调。NO诱导子宫静止,这被认为是维持妊娠所必需的。已知松弛素可促进子宫静止。松弛素还被证明能刺激多个靶器官产生NO。在本研究中,我们调查了松弛素对小鼠子宫NO生物合成途径的影响。用松弛素(2微克)处理雌激素化的小鼠18小时,然后将子宫角用于测定免疫反应性内皮型NOS和诱导型NOS。此外,将雌激素化小鼠的子宫条置于器官浴中,在存在或不存在NOS抑制剂硝基-L-精氨酸的情况下评估松弛素对K+诱导的挛缩的影响。松弛素增加表面上皮、腺体、子宫内膜基质细胞和子宫肌层中内皮型NOS的表达,而诱导型NOS的表达不受影响。此外,松弛素抑制子宫肌层收缩力,并且这种作用被硝基-L-精氨酸减弱,从而表明L-精氨酸-NO途径参与了松弛素对子宫肌层的松弛作用。由于怀孕期间松弛素水平升高,提示松弛素在怀孕期间子宫NO生物合成上调中具有生理作用。

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