Goetz R M, Morano I, Calovini T, Studer R, Holtz J
Institute of Pathophysiology, University of Halle, Germany.
Biochem Biophys Res Commun. 1994 Nov 30;205(1):905-10. doi: 10.1006/bbrc.1994.2750.
The mechanisms underlying enhanced vascular reactivity in pregnancy are not yet defined. In this study we have investigated the potential role of endothelium-derived vasodilator nitric oxide (EDNO). EDNO-mediated dilatory responses in vitro were markedly increased in aorta of pregnant as compared with nonpregnant rats. This increase in EDNO-releasability was accompanied by a two-fold increase in mRNA of endothelial constitutive nitric oxide synthase (NOS-III). Chronically substituted estrogen, but neither progesterone nor testosterone induced an upregulation of NOS-III mRNA in aorta of gonadectomized rats which amounted to about half that induced in aorta of pregnant rats. Thus, increased EDNO-releasability and increased NOS-III mRNA contribute to enhanced vascular reactivity in pregnancy.
孕期血管反应性增强的潜在机制尚未明确。在本研究中,我们探究了内皮源性血管舒张因子一氧化氮(EDNO)的潜在作用。与未孕大鼠相比,孕鼠主动脉中EDNO介导的体外舒张反应显著增强。EDNO释放能力的这种增强伴随着内皮型一氧化氮合酶(NOS-III)mRNA增加两倍。长期给予雌激素替代治疗,但给予孕酮或睾酮均未诱导去性腺大鼠主动脉中NOS-III mRNA上调,其上调程度约为孕鼠主动脉中诱导水平的一半。因此,EDNO释放能力增加和NOS-III mRNA增加促成了孕期血管反应性增强。