Altered Vascular Reactivity of the Cerebral Arteries in Ovariectomized Rat

Abstract

Estrogen has received considerable attention recently as a potential therapeutic agent in vascular pathophysiological states such as stroke. The mechanisms by which estrogen influences cerebral arteries are incompletely understood. The present study was to examine the effect of ovariectomy and chronic estrogen or tamoxifen treatment on vascular reactivity in rat posterior communicating cerebral arteries with intact endothelium. Changes in vascular tension were measured by microvessel myograph. Ovariectomy significantly enhanced the constricting responses to endothelin I, but not to phenylephrine. Chronic treatment with estrogen or tamoxifen partially reversed or abolished the effect of ovariectomy. The contraction induced by high K+ solution was also enhanced in the ovariectomized rats and this enhancement was abolished by estrogen or tamoxifen treatment. Ovariectomy potentiated the relaxant response to nicardipine but not NS 1619. Estrogen but not tamoxifen reversed the effect of ovariectomy. The present results indicate that chronic tamoxifen may not act as an antagonist of estrogen, instead, chronic treatment with estrogen and tamoxifen has similar effect in inhibiting the increased vascular tension induced by ovariectomy. This study suggests the influence of physiological level of estrogen on vascular contractility. It is at present unknown what may have caused increased relaxant effect of nicardipine, a L-type Ca2+ channel blocker. More experiments are needed to show the role of endothelium in the altered vascular contractility in the ovariectomized and estrogen-treated rats. (supported by UPGC Direct Grant).