The female sex steroid, estradiol 17β, mediates its effect through its association with
estrogen receptor present in the target cell. So far the major emphasis has been given to the …

Clinical observations suggest that human breast tumors can adapt to endocrine therapy by
developing hypersensitivity to estradiol (E (2)). To understand the mechanisms responsible …

Background—Estrogen acutely activates endothelial nitric oxide synthase (eNOS). However,
the identity of the receptors involved in this rapid response remains unclear. Methods and …

The cerebral vasculature is an important target tissue for estrogen, as evidenced by
significant effects of estrogen on vascular reactivity and protein levels of endothelial nitric …

Background—Experimental evidence suggests that estrogens stimulate the production of
nitric oxide (NO) by vascular endothelial cells. This effect has been attributed to increased …

Objective—Nontranscriptional signaling mechanisms mediate some of the biological effects
of estrogen, such as the rapid actions on the blood vessels. By interacting with …

We have investigated the involvement of the endothelium, K+ channels, oestradiol
receptors, and Ca2+ influx in 17β-oestradiol-induced vasorelaxation in rat mesenteric …

It is well established that the area postrema, as a circumventricular organ, is susceptible to
modulation by circulating hormones and peptides. Furthermore, activation of the area …

Abstract Estrogen 17β-estradiol (E2) rapidly modulates several signaling pathways related
to cell growth, preservation, and differentiation. The physiological role of these nongenomic …

Estrogens influence the independent cardiovascular risk factor homocysteine as well as
vasodilatation. Homocysteine alone also influences vasodilatation, indicating a relational …