Koga Miho, Hirano Katsuya, Nishimura Junji, Nakano Hitoo, Kanaide Hideo
Division of Molecular Cardiology, Research Institute of Angiocardiology, Graduate School of Medical Sciences, Kyushu University, 3-1-1 Maidashi, Higashi-ku, Fukuoka 812-8582, Japan.
J Soc Gynecol Investig. 2004 Jul;11(5):272-9. doi: 10.1016/j.jsgi.2004.03.002.
Estrogen suppresses contractile response and increases vasodilator response, partly by modulating endothelial function. However, the effect of estrogen on the contractility of vascular smooth muscle remains to be elucidated. We investigated the effect of a long-term estrogen deficiency on vascular contractility and the Ca(2+) sensitivity of the contractile apparatus in arterial smooth muscle.
Female rabbits were divided into the following three groups: control group, an ovariectomized group (OVX), and a group supplemented with 17beta-estradiol after ovariectomy (OVX+E2). Twelve weeks later, the mesenteric artery was isolated, and the vascular contractility was evaluated.
In OVX, the contractile responses to phenylephrine and 118 mM potassium were enhanced, and the basal release of nitric oxide decreased in the strips with endothelium compared with either OVX+E2 or control. An enhancement of contraction was also observed in the strips without endothelium. However, the extent of enhancement was smaller than that observed in the presence of endothelium. The simultaneous measurement of calcium (Ca(2+)) and tension revealed no significant difference in the Ca(2+) elevations induced by phenylephrine among the three groups. In the alpha-toxin permeabilized strips, the Ca(2+)-tension relationships obtained both with and without phenylephrine and guanosine triphosphate were similar among the three groups. No difference in the myosin expression and the histology of vascular tissue was observed among the three groups.
Long-term estrogen deficiency increased the vascular tone mainly by enhancing smooth muscle contractility. Endothelial dysfunction is considered to play a minor role in the augmentation of vascular tone.
雌激素可抑制收缩反应并增强血管舒张反应，部分是通过调节内皮功能实现的。然而，雌激素对血管平滑肌收缩性的影响仍有待阐明。我们研究了长期雌激素缺乏对动脉平滑肌血管收缩性及收缩装置钙（Ca2+）敏感性的影响。
将雌性兔分为以下三组：对照组、去卵巢组（OVX）和去卵巢后补充17β-雌二醇组（OVX+E2）。12周后，分离肠系膜动脉并评估血管收缩性。
与OVX+E2组或对照组相比，OVX组中，对去氧肾上腺素和118 mM钾的收缩反应增强，且有内皮的血管条中一氧化氮的基础释放减少。在无内皮的血管条中也观察到收缩增强。然而，增强程度小于有内皮时观察到的程度。同时测量钙（[Ca2+]i）和张力发现，三组中去氧肾上腺素诱导的[Ca2+]i升高无显著差异。在α-毒素通透的血管条中，三组中在有和没有去氧肾上腺素及三磷酸鸟苷情况下获得的Ca2+ - 张力关系相似。三组之间在肌球蛋白表达和血管组织组织学方面未观察到差异。
长期雌激素缺乏主要通过增强平滑肌收缩性增加血管张力。内皮功能障碍被认为在血管张力增加中起次要作用。
