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Cited by 81Hormonal and reproductive studiesNitric Oxide and Endothelin EffectsEicosanoids and Hypertension Pharmacology

Effect of testosterone on ex vivo vascular reactivity in man

Malkin, Christopher J., Jones, Richard D., Jones, T. Hugh, Channer, Kevin S.·2006·Clinical Science
DOI 10.1042/cs20050354
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Abstract

Testosterone is reported to have an acute vasodilating action in vitro, an effect that may impart a favourable haemodynamic response in patients with chronic heart failure. However, the effect of chronic testosterone exposure on general vascular reactivity is poorly described. In the present study, fresh subcutaneous resistance arteries were obtained from patients with heart failure (n=10), healthy controls (n=9) and men with androgen-deficiency (n=17). All arteries were studied using a wire myograph to examine the effect of cumulative additions of testosterone (1 nmol/l–100 μmol/l) compared with vehicle control following maximal pre-constriction with KCl (1–100 μmol/l). The vascular reactivity of arteries from androgen-deficient patients was examined further by recording tension concentration curves to cumulative additions of noradrenaline (1 nmol/l–100 μmol/l) and U46619 (1–300 nmol/l), followed by relaxation concentration curves to additions of ACh (acetylcholine; 10 nmol/l–30 μmol/l) and SNP (sodium nitroprusside; 10 nmol–30 μmol/l) respectively. In all cases, statistical analysis was performed by ANOVA. Patients with proven androgen-deficiency were treated according to clinical recommendations for a minimum of 3 months and further arteries (n=19) were taken for experimentation using the same protocol. In all groups, testosterone was confirmed to be an acute concentration-dependent vasodilator at concentrations ≥1 μmol/l (P=0.0001). The dilating effect of testosterone was augmented in patients with androgen-deficiency prior to treatment, and this effect was abrogated following appropriate testosterone replacement. Testosterone therapy significantly reduced the normal vascular dilating response to ACh and SNP (P<0.01) and significantly increased the contractile response to noradrenaline (P<0.01), but not U46619. Testosterone is an acute dose-dependent vasodilator of resistance arteries. Physiological testosterone replacement attenuates general vascular reactivity in androgen-deficient subjects. The numerous perceived benefits of testosterone replacement may be offset by a decline in vascular reactivity and, therefore, further studies and careful monitoring of patients is recommended.

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Crossref · 10.1042/cs20050354

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  • Genomic and non-genomic effects, androgen receptor polymorphism, and intracellular steroid metabolism further contribute to the diversity of the time-course of testosterone effects.

    “Genomic and non-genomic effects, androgen receptor polymorphism and intracellular steroid metabolism further contribute to such diversity.”

    From Onset of effects of testosterone treatment and time span until maximum effects are achieved (2011) · cites this paper as [7]

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Authors
Malkin, C. J., Jones, R. D., Jones, T. H., & Channer, K. S.
Affiliations
  • Royal Hallamshire Hospital (GB)
  • University of Sheffield (GB)
ORCID
Venue
Clinical Science
Publisher
Portland Press Ltd.
Published
2006-09-13
Volume
111
Issue
4
Pages
265-274
ISSN
  • 0143-5221 (ISSN-L)
  • 1470-8736
DOI
10.1042/cs20050354
OpenAlex
W1971226227
Cited by
81
References
35
Citations by year
2026: 1 · 2025: 2 · 2023: 4 · 2022: 2 · 2021: 1 · 2020: 1 · 2019: 2 · 2018: 2 · 2017: 1 · 2016: 4 · 2015: 2 · 2014: 6 · 2013: 5 · 2012: 12
FWCI
5.10
Type
journal article
Language
en
Open access
closed
Locations
  • Clinical Science (publishedVersion)
  • PubMed (publishedVersion)
Topics
  • Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Hormonal and reproductive studies
  • Health Sciences › Medicine › Physiology › Nitric Oxide and Endothelin Effects
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Biochemistry › Eicosanoids and Hypertension Pharmacology
Keywords
testosterone, vascular reactivity, resistance arteries, androgen deficiency, testosterone replacement therapy, vasodilation, chronic heart failure, norepinephrine-induced contraction, acetylcholine-induced relaxation, sodium nitroprusside, U46619
MeSH terms
Acetylcholine, Adult, Aged, Arteries, Connective Tissue, Cross-Sectional Studies, Dose-Response Relationship, Drug, Heart Failure, Humans, Hypogonadism, Male, Middle Aged, Myography, Nitroprusside, Norepinephrine, Testosterone, Vasoconstrictor Agents, Vasodilation, Vasodilator Agents, 15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5,13-dienoic Acid

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