The influence of testosterone upon vascular reactivity

Jones, Richard D.; Jones, T. H.; Channer, Kevin S.

doi:10.1530/eje.0.1510029

Cited by 105 publications

(73 citation statements)

References 52 publications

(71 reference statements)

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“…Furthermore, it appears that the effect of testosterone on the vascular system may have an indirect component through the secretion of this vasodilator peptide. These results may partly explain observations that there is an inverse relationship between testosterone concentrations and blood pressure in men and that there can be beneficial effects of testosterone on the vasculature (Khaw & Barrett-Connor 1988, Jones et al 2004.…”

Section: Discussionmentioning

confidence: 70%

Regulation of adrenomedullin release from human endothelial cells by sex steroids and angiotensin-II

Lj¹,

Rait²,

Nicholls³

et al. 2006

Journal of Endocrinology

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It is well documented that there are gender differences in the incidence and patterns of cardiovascular diseases but the reasons are unclear. Sex steroids may modulate the behaviour of vascular endothelial cells, which in turn act by paracrine processes to alter adjacent vascular smooth muscle activity. We hypothesised that the sex steroids alter the percentage of vascular endothelial cells that secrete the vasodilator peptide, adrenomedullin and modify the adrenomedullin-stimulating action of angiotensin-II. The percentage of adrenomedullinsecreting human aortic endothelial cells was determined using the cell immunoblot method. Cells were incubated with selected concentrations of angiotensin-II, oestradiol and testosterone alone and sex steroids in combination with angiotensin-II. Adrenomedullin mRNA expression in endothelial cells was quantified by real-time PCR. It was observed that at 4 h, angiotensin-II increased the percentage of adrenomedullin-secreting cells in a concentration-dependent manner. Testosterone at physiological concentrations was observed to increase the number of adrenomedullin-secreting cells whilst oestradiol had no effect. Addition of testosterone to angiotensin-II resulted in less than additive increases in the number of cells secreting adrenomedullin. Oestradiol reduced the angiotensin-II-induced increase in adrenomedullinsecreting cells. Adrenomedullin mRNA expression was significantly increased by testosterone and there was also a trend for an increase in adrenomedullin mRNA expression, which occurred when cells were incubated with angiotensin-II. Our results point to a complex interplay between the sex steroids and angiotensin-II in regulating adrenomedullin production by human endothelial cells, which may contribute to gender-related differences in vascular disease in humans.

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Section: Discussionmentioning

confidence: 70%

Regulation of adrenomedullin release from human endothelial cells by sex steroids and angiotensin-II

Lj¹,

Rait²,

Nicholls³

et al. 2006

Journal of Endocrinology

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“…77 FMD was increased with short-term physiological and acute supraphysiological testosterone treatments in middleaged men with underlying coronary artery disease. 78 In contradiction to the above data suggesting that testosterone has either a neutral or beneficial effect on vascular reactivity, men undergoing androgen deprivation for prostate cancer show increased 85 Placebo-controlled studies in which serum testosterone was increased within the healthy young adult male normal range showed minimal effects on total and LDL cholesterol and triglycerides, although the decline in HDL cholesterol levels was significant in two of four studies of 12 months or longer 86 (Table 3). Oxandrolone was associated with unfavourable lipid changes.…”

Section: Relationship Of Endogenous Testosterone To Markers Of Cardiomentioning

confidence: 91%

Body composition, metabolic syndrome and testosterone in ageing men

Allan¹,

Strauss

McLachlan

2007

Int J Impot Res

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The ageing process in men is marked by changes in body composition (loss of fat-free mass (FFM) and skeletal muscle, and gain in fat mass (FM)) and is associated with a decline in serum testosterone. Correlations between these aspects of ageing and the acknowledged role of exogenous testosterone in reversing the loss of FFM and gain in FM seen in adult men with congenital or acquired hypoandrogenism have led to the hypothesis that testosterone therapy in ageing men will result in favourable changes in body composition and may improve metabolic status and/or cardiovascular risk. Data from randomized controlled trials of testosterone therapy in ageing men addressing the endpoints of body composition and components of the metabolic syndrome and cardiovascular risk factors are reviewed, and the impact of the increasing prevalence of obesity on these relationships is considered.

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“…One of the interesting factors is the proposed interaction between androgens and endothelial nitric oxide (NO; Tep-areenan et al 2003, Jones et al 2004. In this regard, most studies have been focused on analysing the effects of androgenic derivatives on different aspects of the NO system, such as endothelial nitric oxide synthase (eNOS) expression, NO release or NO vasodilator effect (Hutchison et al 1997, Ceballos et al 1999, Teoh et al 2000.…”

Section: Introductionmentioning

confidence: 99%

Protein kinase C activation increases endothelial nitric oxide release in mesenteric arteries from orchidectomized rats

Blanco-Rivero¹,

Sagredo²,

Balfagón³

et al. 2007

Journal of Endocrinology

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The aim of the present study was to assess the effect of endogenous male sex hormones on endothelial nitric oxide synthase (eNOS) expression, release and function of the endothelial nitric oxide (NO), as well as to assess the regulatory action of protein kinase C (PKC) on acetylcholine (ACh)-induced endothelial NO release. For this purpose, superior mesenteric arteries from control and orchidectomized male Sprague-Dawley rats were used. eNOS expression and basaland ACh-induced NO release were similar in arteries from both groups of rats. Orchidectomy decreased the vasodilator effect induced by ACh but did not alter that induced by sodium nitroprusside (SNP). The superoxide anion scavenger, superoxide dismutase (SOD), or the membrane-permeable mimetic of SOD, tempol, only enhanced ACh-induced relaxation in arteries from orchidectomized rats. ACh-induced TXA 2 formation was higher in arteries from orchidectomized than from control rats. Neither the PKC activator, phorbol 12,13-dibutyrate (PDBu), nor the non-selective PKC inhibitor, calphostin C, modified basal-or ACh-induced NO release in arteries from control rats. In arteries from orchidectomized rats, basal-and ACh-induced endothelial NO release were increased by PDBu but decreased by calphostin C. Both Gö 6976, a PKC inhibitor that is partially selective for conventional PKC isoforms, as well as PKCz pseudosubstrate inhibitor (PKCz-PI) decreased both basal-and ACh-induced NO release in arteries from orchidectomized rats. Neither PDBu nor calphostin C modified the vasodilator response induced by ACh in arteries from control rats. In segments from orchidectomized rats, PDBu enhanced the ACh-induced response, but this response was not modified by calphostin C, Gö6976 or PKCz-PI. The vasodilator response induced by SNP was not altered by the PKC activators or inhibitors in any artery from either group. These results show that endogenous male sex hormone deprivation does not affect the eNOS expression or the endothelial NO release induced by ACh, but does decrease the vasodilator action of ACh, by increasing NO metabolism and TXA 2 formation. In addition, PKC seems to modulate eNOS activity only in mesenteric arteries from orchidectomized rats, in which conventional and PKCz isoforms are involved in the positive regulation of eNOS.

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The influence of testosterone upon vascular reactivity

Cited by 105 publications

References 52 publications

Regulation of adrenomedullin release from human endothelial cells by sex steroids and angiotensin-II

Regulation of adrenomedullin release from human endothelial cells by sex steroids and angiotensin-II

Body composition, metabolic syndrome and testosterone in ageing men

Protein kinase C activation increases endothelial nitric oxide release in mesenteric arteries from orchidectomized rats

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