Testosterone is a potent inhibitor of L-type Ca2+ channels

Scragg, Jason L.; Jones, Richard D.; Channer, Kevin S.; Jones, T Hugh; Peers, Chris

doi:10.1016/j.bbrc.2004.04.054

Cited by 156 publications

(120 citation statements)

References 23 publications

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“…Testosterone has also been shown to inhibit L-type calcium channels via an AR-independent pathway, indicating nongenomic action of androgen on vasodilatation (Scragg et al 2004, Hall et al 2006. However, we have found that there is no difference in blood pressure between male ARKO and age-matched WT mice at 6 months of age (Ikeda et al 2005).…”

Section: Androgens and Hypertensionmentioning

confidence: 54%

Effects of androgens on cardiovascular remodeling

Ikeda

Aihara

Yoshida³

et al. 2012

Journal of Endocrinology

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Androgens, the male sex hormones, exert various biological effects on many target organs through the transcriptional effects of the nuclear androgen receptor (AR). ARs are expressed not only in classical target organs, such as the brain, genital organs, bone, and skeletal muscles, but also in the cardiovascular system. Because the female sex hormones estrogens are wellknown to protect against cardiovascular disease, sex has been considered to have a significant clinical impact on cardiovascular mortality. However, the influence of androgens on the cardiovascular system has not been fully elucidated. To clarify this issue, we analyzed the effects of administration of angiotensin II and doxorubicin, an anticancer agent, in a loading model in male wild-type and AR-deficient mice. In this review, we focus on the actions of androgens as potential targets for the prevention of cardiovascular diseases in males.

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Section: Androgens and Hypertensionmentioning

confidence: 54%

Effects of androgens on cardiovascular remodeling

Ikeda

Aihara

Yoshida³

et al. 2012

Journal of Endocrinology

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“…Similar results have been reported in different experimental conditions by other groups. [106][107][108] The involvement of potassium channels in testosterone-induced vasodilatation has also been studied by many researchers. [109][110][111] Cairrao et al 112 reported that an AR antagonist, flutamide, and an adenosine triphosphate-sensitive potassium-channel inhibitor, glibenclamide, had no influence on the testosterone relaxant effect, whereas a voltage-sensitive potassium-channel inhibitor, 4-aminopyridine, decreased this effect of testosterone.…”

Section: Effects Of Testosterone On Ecsmentioning

confidence: 99%

Hormonal effects on blood vessels

Akishita

2012

Hypertens Res

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The incidence of cardiovascular disease (CVD) is lower in younger women than in men of the same age, but it increases after menopause, implicating the atheroprotective action of endogenous estrogen. Although observational studies have suggested the efficacy of estrogen therapy in postmenopausal women, placebo-controlled, randomized trials, such as the Women's Health Initiative, have not confirmed effects of estrogen therapy on CVD. Conversely, basic, experimental research has progressed and provided mechanistic insight into estrogen's action on blood vessels. By contrast, the vascular effects of androgens remain poorly understood and have been controversial for a long time. In recent years, an increasing body of evidence has suggested that androgens may exert protective effects against the development of atherosclerosis, at least in elderly men. Epidemiological studies have shown that the incidence of and mortality due to CVD were increased in elderly men with low testosterone levels, although the efficacy of androgen therapy remains unknown. Furthermore, recent experimental studies have demonstrated the direct action of androgens on the vasculature. In this review, we illustrate the effects of sex steroids on the cardiovascular system, focusing on the action of testosterone on the blood vessels.

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“…In addition to these trophic effects through transcriptional regulation, androgens may also regulate vascular smooth muscle contractility by nongenomic mechanisms, such as relaxation of coronary arteries by activating potassium channels and inhibiting calcium channels. 23 Reilly et al…”

Section: Basic Research On T and Erectile Functionmentioning

confidence: 99%

The relationship between hypogonadism and erectile dysfunction

Hwang

Lin

2008

Int J Impot Res

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It is well known that testosterone enhances sexual interest leading to an increased frequency of sexual acts and an increase in the frequency of sleep-related erections. However, it has little effect on fantasy-or visually induced erections. Exact contribution to erection from testosterone in men remains unclear. Animal studies have well demonstrated that testosterone plays critical physiological (activity of nitric oxide synthases and phosphodiesterases), biochemical (through an endothelial-independent pathway and adrenergic tonicity) and structural (change of fibroelasticity and hollow cell accumulation) roles in erectile function. The supplementation of testosterone to castrated animals can restore erectile function. Clinically, reports of patients with erectile dysfunction (ED) combined with hypogonadism who receive testosterone therapy have inconsistent results. However, testosterone may ameliorate the expression of the phosphodiesterase-5 (PDE5) inhibitor, and the use of testosterone in conjunction with the PDE5 inhibitor revealed convincing results. Because of potential risks in clinical use, testosterone therapy should be individualized, carefully considered and closely monitored, especially, in patients with possible occult prostate cancer, and large benign prostatic hyperplasia. Lower urinary tract symptoms might be worsened by this treatment, since the prostate is an androgen-dependent tissue.

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Testosterone is a potent inhibitor of L-type Ca2+ channels

Cited by 156 publications

References 23 publications

Effects of androgens on cardiovascular remodeling

Effects of androgens on cardiovascular remodeling

Hormonal effects on blood vessels

The relationship between hypogonadism and erectile dysfunction

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