Sex hormone replacement therapy and modulation of vascular function in cardiovascular disease

Koledova, Vera V.; Khalil, Raouf A.

doi:10.1586/14779072.5.4.777

Cited by 36 publications

(41 citation statements)

References 80 publications

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“…Additionally, Bhasin et al (2010) recommend testosterone therapy only for men with consistent symptoms of androgen deficiency and unequivocally low serum testosterone levels. These researchers author found controversial results from androgenic therapies depending of the age of the patients (Spitzer et al, 2013), and this result is in agreement with the observations reported by Koledova and Khalil (2007). However, these researchers found that the administration of T with low-intensity physical training improves grip strength, spontaneous movements, and respiratory activity.…”

Section: Risks and Benefits Of Replacement Therapy With Sex Hormones:supporting

confidence: 79%

“…Another therapeutic approach may involve the use of specific ER modulators (SERMs), which minimize the adverse effects of HRT, including breast cancer. Thus, the beneficial effects of HRT in postmenopausal vascular disease can be enhanced by customizing the HRT type, dose, route of administration, and timing depending on the subject's age (Koledova and Khalil, 2007). Therefore, the use of specific phytoestrogens or SERMS as an alternative therapy could be employed to correct alterations of estrogen deficiency or to decrease malignancy outcomes if these compounds are prescribed correctly.…”

Section: Risks and Benefits Of Replacement Therapy With Sex Hormones:mentioning

confidence: 99%

See 1 more Smart Citation

Actions of 17β-estradiol and testosterone in the mitochondria and their implications in aging

Vasconsuelo¹,

Milanesi²,

Boland³

2013

Ageing Research Reviews

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Section: Risks and Benefits Of Replacement Therapy With Sex Hormones:supporting

confidence: 79%

Section: Risks and Benefits Of Replacement Therapy With Sex Hormones:mentioning

confidence: 99%

Actions of 17β-estradiol and testosterone in the mitochondria and their implications in aging

Vasconsuelo¹,

Milanesi²,

Boland³

2013

Ageing Research Reviews

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“…32 Furthermore, several studies have shown different effects of different progestins on endothelial function and thrombotic risk. [32][33][34][35] The WHI study has shown that in nonhysterectomized women receiving CEE-MPA in continuous combined scheme increased cardiovascular events in elderly PMW, whereas this was not the case in women receiving CEE alone. 10,11 Limitations of the present study are the lack of placebo control and of the adjunctive use of progestins.…”

Section: Discussionmentioning

confidence: 99%

Time Since Menopause Influences the Acute and Chronic Effect of Estrogens on Endothelial Function

Vitale

Mercuro

Cerquetani

et al. 2008

ATVB

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Objective-We evaluated whether time since menopause influences the acute and chronic effect of Estradiol (E) on vascular endothelial function. Methods and Results-We studied flow-mediated dilatation (FMD) in 134 postmenopausal women (PMW) before and after acute and chronic E administration. At baseline FMD was inversely associated to time from menopause (rϭϪ0.67, PϽ0.001) and age (rϭϪ0.43, PϽ0.05), in exogenous estrogen naïve but not in previous users. Acute and chronic E improved endothelial function in all women. E administration improved FMD more in women within 5 years since menopause than in those with more than 5 years since menopause (76% and 74% versus 45% and 48%, acute and chronic E, respectively; PϽ0.05). Among women with more than 5 years since menopause acute and chronic E increased FMD more in previous E users than in nonusers (59% and 63% versus 31% and 38%, acute and chronic E, respectively; PϽ0.01). Multivariate analysis showed that time from menopause was a predictor of impaired FMD and of its improvement after acute and chronic E. Key Words: endothelium Ⅲ endothelial function Ⅲ cardiovascular disease prevention Ⅲ risk factors Ⅲ estrogen E ndothelial dysfunction is an initial step in the development of atherosclerosis and is associated with the progression of atherosclerosis and with cardiovascular events in men and women. 1 Although aging is associated independently with a progressive decline in endothelium-dependent vasodilatation in both sexes, 2-3 age-related endothelial dysfunction is attenuated in premenopausal women, compared with men of similar age. However, no difference in endothelial function between sexes is observed after the 5 th decade, suggesting a protective effect of endogenous ovarian hormones on endothelial function in women. 2,4 -6 Several studies have shown that estrogen or estrogenprogestin replacement therapy (ERT or HRT) restore, at least in part, the impairment of endothelial function related to the cessation of menses. [7][8] In spite of a large body of evidence suggesting favorable effects of estrogens alone or in combination with progestins on surrogate markers of cardiovascular disease and on cardiovascular events, recent randomized controlled trials (RCT) failed to show a significant reduction in cardiovascular events with ERT or HRT in predominantly late postmenopausal women (PMW). 9 -12 It has been suggested that the discrepancy between observational and RCT may be dependent on the timing of the initiation of ERT or HRT and on the different cardiovascular effects of ovarian hormones in younger and older women. [13][14][15][16] Recent studies have suggested that the vascular effect of ERT or HRT is age dependent 17 ; however, it is not known whether the vascular effect of estrogens is related purely to age or more to the duration of estrogen deficiency and whether previous exposure to ERT may influence the vasodilator effect of estrogens in women. Conclusions-TimeThe aim of the present study was to evaluate the effect of time since menopause and previous hormon...

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“…A great deal of evidence from observational and experimental studies, in both animals and humans, supports the concept of a protective effect of estrogens on the cardiovascular system (Koledova & Khalil 2007). Thus, it was wholly unexpected when the Women's Health Initiative, a large-scale trial of hormone replacement therapy (HRT) in postmenopausal women, was terminated early due to a surprising increase in the incidence of cardiovascular events (Hsia et al 2006).…”

Section: Introductionmentioning

confidence: 99%

Testosterone modulates platelet aggregation and endothelial cell growth through nitric oxide pathway

Campelo¹,

Cutini²,

Massheimer³

2012

Journal of Endocrinology

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The aim of the present study was to investigate the effect of testosterone on the modulation of cellular events associated with vascular homeostasis. In rat aortic strips, 5-20 min treatment with physiological concentrations of testosterone significantly increased nitric oxide (NO) production. The rapid action of the steroid was suppressed by the presence of an androgen receptor antagonist (flutamide). We obtained evidence that the enhancement in NO synthesis was dependent on the influx of calcium from extracellular medium, because in the presence of a calcium channel blocker (verapamil) the effect of testosterone was reduced. Using endothelial cell (EC) cultures, we demonstrated that androgen directly acts at the endothelial level. Chelerythrine or PD98059 compound completely suppressed the increase in NO production, suggesting that the mechanism of action of the steroid involves protein kinase C and mitogen-activated protein kinase pathways. It is known that endothelial NO released into the vascular lumen serves as an inhibitor of platelet activation and aggregation. We showed that testosterone inhibited platelet aggregation and this effect was dependent on endothelial NO synthesis. Indeed, the enhancement of NO production elicited by androgen was associated with EC growth. The steroid significantly increased DNA synthesis after 24 h of treatment, and this mitogenic action was blunted in the presence of NO synthase inhibitor N-nitro-L-arginine methyl ester. In summary, testosterone modulates vascular EC growth and platelet aggregation through its direct action on endothelial NO production.

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Sex hormone replacement therapy and modulation of vascular function in cardiovascular disease

Cited by 36 publications

References 80 publications

Actions of 17β-estradiol and testosterone in the mitochondria and their implications in aging

Actions of 17β-estradiol and testosterone in the mitochondria and their implications in aging

Time Since Menopause Influences the Acute and Chronic Effect of Estrogens on Endothelial Function

Testosterone modulates platelet aggregation and endothelial cell growth through nitric oxide pathway

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