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Abstract
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.
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