Barron Carolyn, Mandala Maurizio, Osol George
Department of Obstetrics, Gynecology, and Reproductive Sciences, University of Vermont College of Medicine, Burlington, VT 05405, USA.
J Vasc Res. 2010;47(6):463-71. doi: 10.1159/000313874. Epub 2010 Apr 30.
BACKGROUND/AIMS: The purpose of this study was to examine the effects of hypertension and nitric oxide (NO) inhibition on myogenic tone in uterine arteries during pregnancy.
Premyometrial radial uterine arteries from nonpregnant and late pregnant Sprague-Dawley rats were evaluated for myogenic reactivity from the following groups: control, hypertensive/NO-inhibited (L-NAME treatment) and normotensive/NO-inhibited (L-NAME plus hydralazine).
In both nonpregnant and pregnant animals, L-NAME treatment significantly elevated blood pressures, while the addition of hydralazine made the animals normotensive. In nonpregnant animals, little myogenic tone was seen in controls; tone increased significantly in the L-NAME group, and was attenuated in those treated with L-NAME plus hydralazine. In pregnant animals, controls developed significant tone; this was reduced in the L-NAME group, and returned to control levels in the L-NAME plus hydralazine group.
Dimensional measurements showed that arteries from the pregnant hypertensive group did not undergo expansive remodeling, suggesting that tone development is related to phenotypic alterations in vascular smooth muscle and/or altered physical forces secondary to adaptive changes in arterial diameter. These differences implicate pregnancy-specific pathways in the development and inhibition of myogenic tone, and point to potentially opposing roles of NO and hypertension.
背景/目的:本研究旨在探讨高血压和一氧化氮(NO)抑制对孕期子宫动脉肌源性张力的影响。
对来自未孕和孕晚期的Sprague-Dawley大鼠的子宫肌层前径向子宫动脉进行评估,观察以下几组的肌源性反应:对照组、高血压/NO抑制组(L-NAME处理)和正常血压/NO抑制组(L-NAME加肼屈嗪)。
在未孕和孕鼠中,L-NAME处理均显著升高血压,而添加肼屈嗪可使动物血压恢复正常。在未孕动物中,对照组几乎未见肌源性张力;L-NAME组张力显著增加,而L-NAME加肼屈嗪处理组的张力减弱。在孕鼠中,对照组出现显著张力;L-NAME组张力降低,而L-NAME加肼屈嗪组张力恢复至对照水平。
尺寸测量显示,妊娠高血压组的动脉未发生扩张性重塑,提示张力的产生与血管平滑肌的表型改变和/或动脉直径适应性变化继发的物理力改变有关。这些差异表明,在肌源性张力的产生和抑制过程中存在妊娠特异性途径,并提示NO和高血压可能具有相反的作用。