Effect of Estradiol 17β on Pressor Responses of Rat Mesenteric Bed to Norepinephrine, K+, and U-46619

Publisher Website
Google Scholar
Abstract
Summary We reinvestigated the effect of estradiol 17β on the responses of adrenergic and nonadrenergic vasoconstrictors characterized it in terms of steroid specificity, time course, and the role of classic estrogen receptors. We evaluated the effect of estradiol 17β on the pressor responses of isolated perfused rat mesenteric vascular bed (McGregor's preparation). Estradiol 17β (7–700 nM) significantly increased the pressor response to bolus applications of norepinephrine (NE) (p < 0.05). However, estradiol 17β did not significantly increase the responses to endogenous NE release induced by electrical field stimulation. Other steroids, testosterone, and the 17α isomer of estradiol (7 and 700 nM) were ineffective. Estradiol 17β (700 nM) also significantly increased the maximum pressor response of rat mesenteric preparation to both the prostaglandin endoperoxide analogue U-46619 and to K+. The potentiation by estradiol 17β of mesenteric vasoconstriction elicited by NE, K+, and U-46619 was rapid (2–8 min), suggesting that a nuclear receptor may not be involved. This notion received further support in that significant potentiation of the NE-induced pressor response was also observed with estradiol 17β conjugated to albumin (700 nM), but not when electrical field stimulation was used. The conjugate increased the effect of all NE concentrations. Its effect was also more consistent (p < 0.01) than that elicited by free estradiol 17β. The dose-response curve was shifted to the left, and the maximum effect was increased. These data suggest that estradiol 17β may possess rapid nongenomic actions unrelated to nuclear receptor binding and gene transcription.

This publication has 0 references indexed in Scilit: