Context. Contribution of endogenous Testosterone (TS) in the functional integrity of peripheral circulation in men.

Objective. Vascular reactivity in male congenital hypogonadal patients before and after prolonged exposure to normal TS levels.

Design. Longitudinal study in which, basically and after 6-months (range 6-8 months) androgen treatment, we investigated forearm blood flow (strain-gauge plethysmography) changes induced by intra-arterial acetylcholine, alone or in presence of L-NMMA infusion, and by sodium nitroprusside. We also evaluated, by Doppler ultrasound, flow-mediated dilation of the brachial artery in response to reactive hyperemia and to glyceryl trinitrate.

Setting. University referral Centers for andrologic and blood-pressure diseases.

Patients. Eight adult male caucasian hypogonadal patients and 9 healthy matched control subjects.

Intervention. Testosterone enanthate (250 mg in 1 ml oily solution) by i.m. injection every 3 weeks.

Results. At baseline, brachial artery diameter and reactive hyperemia, flow-mediated dilation and glyceryl trinitrate responses showed no difference between the two groups. Testosterone therapy increased plasma total testosterone (P < 0.02) and reduced HDL (P < 0.01) and total cholesterol (P < 0.04). It did not affect vasodilation to sodium nitroprusside (355 ± 47%), but it further reduced the vascular response to acetylcholine (187 ± 29%, P < 0.01 vs. baseline) and abolished the inhibition by L-NMMA on acetylcholine (inhibition: 3.2%). Moreover, testosterone therapy decreased (P < 0.01) flow-mediated dilation, while not modifying brachial artery diameter and responses to reactive hyperemia and glyceryl trinitrate.

Conclusions. Hypogonadal patients show impaired vascular reactivity, including endothelial-dependent vasodilation due to reduced nitric oxide availability. Testosterone administration further impairs nitric oxide availability in these patients.