Sex Hormones Affect the Calcium Signaling Response of Human Arterial Cells to LDL

Wells, Kip E.; Miguel, Remedios; Alexander, Robert R.

doi:10.1006/jsre.1996.0224

Cited by 9 publications

(2 citation statements)

References 6 publications

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“…This modulation of TX-A 2 receptor density in VSMC is mediated by DHT (387) and is more prominent in aortic VSMCs from male than from female rats (388). Testosterone has also been shown to directly influence vasoconstriction via regulating Neuropeptide Y1 receptor density (389), while estradiol has a vasodilatory property by increasing PGI 2 production (390) and decreasing cytosolic calcium (391). Each of these may be potential mechanisms responsible for gender differences in vascular function.…”

Section: Effect Of Androgens On Vasomotor Functionmentioning

confidence: 99%

Androgens and Coronary Artery Disease

Wu¹,

Eckardstein²

2003

Androgens in Health and Disease

176

282

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This chapter reviews data that examine the relationship between androgens and coronary artery disease (CAD) in men. Androgens can exert both beneficial and deleterious actions on a myriad of factors implicated in the pathogenic mechanisms of atherosclerosis and CAD.Androgen/androgen receptor (AR) can modulate arterial disease and vascular function via genomic (AR) or non-genomic mechanisms in animal models and in vitro experimental studies. The diversity and complexity of the actions of testosterone (and its metabolites E2 and DHT) and DHEA on the vasculature reflect the multiple cellular targets in the vessel wall, differences between species, gender, concomitant disease and, most importantly, level/dosage of testosterone exposure.At present, it is not possible to determine the net effect of androgens on CAD pathogenesis and clinical outcomes. While observational clinical studies showed a consistent association between low testosterone and CAD (risk factors, events and mortality), and some experimental studies may suggest positive effects of androgens on CAD risk factors, body composition and individual vascular mechanisms, it is hazardous to suggest that manipulation of the androgenic milieu will result in clinical benefits in a complex multifactorial condition such as CAD. This ongoing uncertainty also underlines recent concerns regarding the possibility of adverse cardiovascular side effects in androgen treatment of endocrine and non-endocrine conditions, hampering efforts to exploit the potential therapeutic benefits of testosterone for men in the treatment of osteoporosis, sarcopaenia, chronic debilitating disease and obesity-related hypoandrogenism in the ageing male population. Large-scale prospective randomised placebo-controlled trials of sufficient size and duration are urgently needed to assess not only the benefits in terms of meaningful clinical benefits and patientimportant outcomes but also to document the risks of serious adverse events in testosterone treatment. In the meantime, for patients with established pathological hypogonadism, there are no substantive data to suggest that physiological testosterone therapy is associated with increased cardiovascular risk and their management should not deviate from current recommended practice. For complete coverage of this and related topics, please visit www.endotext.org.

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Section: Effect Of Androgens On Vasomotor Functionmentioning

confidence: 99%

Androgens and Coronary Artery Disease

Wu¹,

Eckardstein²

2003

Androgens in Health and Disease

176

282

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“…However, it is quite possible that the similar actions of estrogens and antioxidants are the result of use of common signal transduction pathways that may be initiated by different processes. [308][309][310][311][312][313]…”

Section: Mechanism(s) By Which Estrogens May Act To Reduce Atherosclementioning

confidence: 99%

Aging, Menopause, and Free Radicals

Schwenke¹

1998

Semin Reprod Med

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As women undergo menopause, circulating concentrations of estrogen decrease. The relative estrogen deprivation in postmenopausal women is associated with physiological changes and increased risk of several diseases, including cardiovascular disease. Studies in animals have shown that exogenous estrogen inhibits atherosclerosis, the underlying cause of cardiovascular disease. Ongoing clinical trials will soon provide data for the effect of exogenous estrogen on cardiovascular disease in postmenopausal women. Estrogen has a number of effects that could influence atherogenesis and cardiovascular disease. Estrogens have favorable effects on lipoproteins, but such effects can only account for part of the protection from cardiovascular disease that appears to be conferred by estrogen. Evidence suggests that estrogens can have both prooxidant and antioxidant effects. However, the available evidence suggests that in vivo physiological concentrations of estrogen may have a modest antioxidant activity, and prooxidant activity is unlikely. The antioxidant activity of estrogens and inhibition by estrogens of cellular processes that are thought to promote atherosclerosis are likely to be additional mechanism(s) by which estrogen inhibits atherosclerosis and cardiovascular disease, but more work is needed. Studies of some effects of estrogens on atherogenic processes in isolated cells need to be extended to the whole animal. The influence of estrogen receptors on inhibition of atherosclerosis by estrogen needs to be clarified. Future studies should be designed to investigate separately the estrogenic and antioxidant activities of estrogens and estrogen analogs. Investigations of the antioxidant activities of estrogens should include careful consideration of the interaction of estrogens with endogenous antioxidants and fatty acid saturation, and more attention should be paid to the potential for estrogens to inhibit intraarterial oxidation.

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