The gender difference in cardiovascular disease has been partly attributed to higher androgenic hormone levels. Although testosterone in women may not affect lipids, it remains unknown whether it negates favorable estrogenic effects on endothelial function. We have investigated the effects of testosterone implant therapy on arterial reactivity encompassing endothelial-dependent and -independent vasodilation in women using hormone replacement therapy (HRT). B-mode ultrasound measurements of resting brachial artery diameter, following reactive hyperemia [endothelium-dependent flowmediated dilation (FMD)] and following glyceryl trinitrate (GTN) (endothelium-independent dilation), were recorded in 33 postmenopausal women stabilized on HRT (Ͼ6 months), at baseline, and 6 weeks after a testosterone implant (50 mg), with 15 postmenopausal nonusers of HRT serving as controls. In the brachial artery, baseline resting diameter was similar (0.40 Ϯ 0.01 vs. 0.41 Ϯ 0.01 cm, P ϭ 0.5). In the treated group, testosterone levels increased (0.99 Ϯ 0.08 to 4.99 Ϯ 0.3 nmol/L, P Ͻ 0.001), associated with a mean 42% increase in FMD (6.4% Ϯ 0.7 to 9.1% Ϯ 1.1, P ϭ 0.03). The control group did not change (8.1% Ϯ 1.4 to 5.6% Ϯ 1.0, P ϭ 0.4). ANOVA of repeated measures (P ϭ 0.04) and mean change (P ϭ 0.02) in FMD both demonstrated significantly greater improvement with testosterone compared with controls. GTN induced vasodilation increased with testosterone treatment (14.9% Ϯ 0.9 to 17.8% Ϯ 1.2, P ϭ 0.03). Our preliminary data indicate that parenteral testosterone therapy improves both endothelial-dependent (flow-mediated) and endothelium-independent (GTN-mediated) brachial artery vasodilation in postmenopausal women using long-term estrogen therapy. The mechanisms underlying these potentially beneficial cardiovascular effects require further investigation. (J Clin Endocrinol Metab 86: 158 -161, 2001) T ESTOSTERONE LEVELS DECLINE with increasing age in women during the reproductive years (1) and acutely following bilateral ovariectomy (2). Increasingly, testosterone is used in hormone replacement regimens to restore libido in postmenopausal women (3-5), with testosterone implants now approved for this purpose in the United Kingdom. Postmenopausal estrogen modulates cardiovascular risk via several mechanisms (6). Whether coadministration of testosterone attenuates these cardioprotective effects or is, in fact, deleterious has not been established. We have previously demonstrated that long-term testosterone implant therapy does not adversely affect the improvements in lipoprotein lipids associated with postmenopausal estrogen use (3). Studies in animals (7, 8), and more recently in men with established coronary artery disease (9), indicate that parenteral testosterone does not adversely affect coronary artery vascular function. However, the effect of parenteral testosterone replacement on vascular reactivity in postmenopausal women has not been reported.Endothelial dysfunction, a putative early marker of vascular disease, can be ...
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