Estrogen replacement reduces PGHS-2-dependent vasoconstriction in the aged rat

被引:16
作者
Armstrong, SJ
Zhang, YL
Stewart, KG
Davidge, ST [1 ]
机构
[1] Univ Alberta, Perinatal Res Ctr, Heritage Med Res Ctr 232, Edmonton, AB T2G 2S2, Canada
[2] Univ Alberta, Dept Obstet Gynecol, Edmonton, AB T2G 2S2, Canada
[3] Univ Alberta, Dept Physiol, Edmonton, AB T2G 2S2, Canada
来源
AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY | 2002年 / 283卷 / 03期
关键词
mesenteric arteries; prostaglandin H synthase; nitric oxide; NS-398;
D O I
10.1152/ajpheart.00148.2002
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
The reduction in estrogen in postmenopausal women contributes to an increase in vascular dysfunction. Models of aging have shown that this is due, in part, to increased prostaglandin H synthase (PGHS)-dependent vasoconstriction. We showed previously that inducible PGHS-2-dependent vasoconstriction is increased with aging. In the present study, we hypothesized that estrogen suppresses PGHS-2-dependent constriction in the aged rat. Isolated mesenteric arteries from placebo- or estrogen-treated, ovariectomized aged (24 mo) Fisher rats were assessed for endothelium-dependent relaxation in the absence or presence of PGHS inhibitors. PGHS inhibition (meclofenamate, 1 mumol/l) enhanced methacholine-induced relaxation only in the placebo group. Specific PGHS-2 inhibition (NS-398, 10 mumol/l) increased arterial relaxation to a greater extent than PGHS-1 inhibition (valeryl salicylate, 3 mmol/l). Estrogen prevented the PGHS-dependent constrictor effect but did not enhance nitric oxide-dependent relaxation in this model. PGHS-1 and endothelial nitric oxide synthase were not altered by estrogen, whereas PGHS-2 expression was decreased in the estrogen-replaced rats (P<0.05). In summary, estrogen replacement improved vasodilation in aged rats by decreasing PGHS-dependent constriction.
引用
收藏
页码:H893 / H898
页数:6
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