Abstract
PurposeTestosterone (T) exerts different effects on the cardiovascular system. Despite this knowledge, the acute vascular effect of androgen remains still poorly understood.MethodsWe investigated the acute effects of T on vascular function in ten men (18–40 years age) with hypogonadism and severe hypotestosteronemia [serum total testosterone (TT) = 0.6 ± 0.3 ng/mL]. In a 4-day double-blind, randomized, placebo-controlled crossover study, we administered 80 mg daily dose of transdermal-T gel (TG) and evaluated endothelial variations with Endopat2000 (reactive hyperemia index, RHI and the augmentation index, AI); also, CAG repeat polymorphism in exon 1 of the androgen receptor gene was investigated.ResultsAfter TG administration, RHI significantly improved at 4 h (p < 0.05), while AI improvement was recorded at 4 and 96 h, also when adjusted for heart rate (AI@75; p < 0.01 and p < 0.001, respectively). Direct relationships between ΔT, ΔDHT and ΔRHI variations (r = 0.37, p < 0.01; r = 0.17, p < 0.05, respectively) as well as between “CAG repeats” length and ΔLnRHI at 96 h (p < 0.03, r2 = 0.47) were found. An inverse relationship between ΔT and ΔAI (p < 0.01, r = −0.35) and ΔAI@75 (p < 0.01, r = −0.38) were found.ConclusionAdministration of TG causes an acute vasodilation and improves arterial stiffness probably due to non-genomic actions of T. Endothelial vasodilatory response was more pronounced depending on higher plasma TT and DHT levels attained. Clinical implications in elderly frail populations are discussed.
Highlights
The endothelium is a single layer of cells that line the luminal surface of blood vessels
We recently demonstrated that long-term T administration in obese hypogonadal men is able to improve metabolic parameters as well as endothelial function and that a 6-month withdrawal reverts most of the beneficial effects [15]
4 and 96 h after starting treatment with T gel (TG), 80 mg daily, serum TT, FT and DHT levels showed a statistically significant increase compared to the basal values for all subjects, (p < 0.0001, p < 0.001 and p < 0.001, respectively; Table 2)
Summary
The endothelium is a single layer of cells that line the luminal surface of blood vessels. In a normal physiologic state, healthy endothelium serves as an anticoagulant membrane, exerting predominantly fibrinolytic, anticoagulant and anti-aggregation effects [1]. The vascular endothelium plays an obligatory role in vasodilation by the action of endothelial-derived nitric oxide (NO). The presence of different cardiovascular risk factors (CRFs), such as aging, smoking, hypertension, dyslipidemia, diabetes, obesity and some less traditional factors (e.g., inflammation, hypoxia, oxidative stress and hyperhomocysteinemia), is known to cause endothelial dysfunction (EDys) [2]. EDys is characterized by significant modifications in the physiological and biochemical parameters in the endothelium. These include: vascular stiffness, increased vascular tone, production of inflammatory cytokines, increased permeability, susceptibility to invasion of immunocytes, decrease in endothelial cell growth and dysregulation of fibrinolytic factors
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