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Articles in PresS, published online ahead of print May 16, 2002
Am J Physiol Heart Circ Physiol, 10.1152/ajpheart.00148.2002
Submitted on February 25, 2002
Accepted on May 13, 2002
1 Departments of Ob/Gyn and Physiology, University of Alberta, Edmonton, Alberta, Canada
* To whom correspondence should be addressed. E-mail: sandra.davidge{at}ualberta.ca.
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 had previously shown that inducible PGHS-2-dependent vasoconstriction is increased with aging. In this 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 months) Fisher rats were assessed for endothelium-dependent relaxation in the absence or presence of PGHS inhibitors. PGHS inhibition (meclofenamate, 1 µmol/L) enhanced methacholine-induced relaxation in only the placebo group. Specific PGHS-2 inhibition (NS-398, 10 µmol/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 while 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.
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