Rapid changes of flow-mediated dilatation after surgical menopause

The Cardiovascular Effects of Chronic Hypoestrogenism in Amenorrhoeic Athletes

“…Blunted circulating levels of nitrite/nitrate [169], in addition to increased plasma levels of endothelin-1 [170], and impaired endothelium-dependent [171] and -independent [172] function occurs in postmenopausal women not receiving E2-or HRT. Further, recent data demonstrate that acute (7 days) E2 deficiency due to ovariectomy is associated with unaffected endothelial function [173], as well as impaired endothelium-dependent, but not -independent vasodilation [162] in response to flow-mediated dilation. The reason for differing findings between these studies [162,173] is not clear.…”

“…Further, recent data demonstrate that acute (7 days) E2 deficiency due to ovariectomy is associated with unaffected endothelial function [173], as well as impaired endothelium-dependent, but not -independent vasodilation [162] in response to flow-mediated dilation. The reason for differing findings between these studies [162,173] is not clear. Taken together these data suggest that reduced circulating levels of E2 may effect impaired endothelialdependent and -independent function, and is associated, in part, with reduced nitric oxide production and/or bioavailability [169].…”

“…Impaired release and/or bioavailability of nitric oxide has been linked with hypertension [156], hypercholesterolemia [157], diabetes [158], tobacco use [159], established coronary artery disease [160], and E2 deficiency [161]. Consequently, factors that decrease nitric oxide production and/or bioavailability may promote atheroslcerosis [162].…”

Does HRT Change İntraocular Pressure in Postmenopausal Women ?

“…Second, the vascular theory suggests that optic nerve degeneration caused by decreased perfusion or vascular dysregulation (5,9,10). (11,12). Additionally, animal models and clinical studies have shown that the perfusion of the optic nerve, retinal ganglion cells, and their supporting structures are increased by estradiol (13)(14)(15).…”

Molecular Mechanism of Action of Selective Estrogen Receptor Modulator in Target Tissues

“…It was found that eNOS is also an Akt substrate and is activated by Akt-dependent phosphorylation to synthesize NO in endothelial cells [17,18]. Recently, we reported that estrogen induces the Aktdependent activation of eNOS in vascular endothelial cells [19], resulting in rapid dilatation of blood vessels [20]. In addition, support for a short-term activation of eNOS, mediated by estrogen receptor-a functioning in a transcription-independent manner, a so-called nongenomic mechanism involving ERK, has recently been published [21].…”