Although estrogen is known to activate endothelial nitric oxide synthase (eNOS) in the
vascular endothelium, the molecular mechanism responsible for this effect remains to be …

OBJECTIVES:: Acute administration of estrogen results in vasodilation and increased nitric
oxide (NO) production. We examined the hypothesis that this is due to activation of Akt/PKB …

17β-Estradiol (E2) is a rapid activator of endothelial nitric oxide synthase (eNOS). The
product of this activation event, NO, is a fundamental determinant of cardiovascular …

Estrogen is an important vasoprotective molecule that causes the rapid dilation of blood
vessels by activating endothelial nitric oxide synthase (eNOS) through an unknown …

Estradiol is known to exert a protective effect against the development of atherosclerosis, but
the mechanism by which this protection is mediated is unclear. Since animal studies strongly …

To determine the mechanism of the antiatherosclerotic effect of estrogen, we investigated
the effect of estrogen on endothelial nitric oxide synthase (NOS-3). Preincubation with a …

17β-Estradiol activates endothelial nitric oxide synthase (eNOS), enhancing nitric oxide
(NO) release from endothelial cells via the phosphatidylinositol 3-kinase (PI3-kinase)/Akt …

Estrogen is an important atheroprotective molecule that causes the rapid dilation of blood
vessels by stimulating endothelial nitric oxide synthase (eNOS). There is also evidence that …

Estrogen causes rapid endothelial nitric oxide (NO) production because of the activation of
plasma membrane-associated estrogen receptors (ER) coupled to endothelial NO synthase …

Rapid uterine vasodilatation after estrogen administration is believed to be mediated by
endothelial production of nitric oxide (NO) via endothelial NO synthase (eNOS). However …