Aim: 

as it seems to be a link between cardiovascular disease, diabetes and low levels of serum testosterone, the aim was: 1) to assess the vasoactive effects of testosterone in rabbit carotid artery; 2) to allocate the vasoactive testosterone concentrations in the physiological or pharmacological range; 3) to assess the involvement of nitric oxide, prostanoids, K⁺-efflux and Ca²⁺-influx in the vasoactive effects of testosterone; and 4) to study the modulating effects of diabetes on testosterone vasoactive effects.

Methods: 

the isometric tension developed by isolated carotid arteries from control and alloxan-induced diabetic rabbits was measured.

Results: 

the concentration-dependent relaxation of norepinephrine-precontracted carotid arteries induced by testosterone (10^-8-3x10^-4 M) in control rabbits resulted increased in diabetic rabbits. In control rabbits neither endothelium removal nor N^G-nitro-L-arginine (10^-5 M) modified the relaxant action of testosterone, and indomethacin (10^-5 M) displaced to the left the concentration-response curve. However, in diabetic rabbits endothelium removal, N^G-nitro-L-arginine (10^-5 M) or indomethacin (10^-5 M) displaced to the right the concentration-response curve to testosterone. Testosterone (10^-4 M) inhibited the contraction to CaCl₂ (10^-5-3x10^-2 M) and this inhibition was lower in diabetic than in control rabbits.

Conclusion: 

diabetes enhances the vasodilator response of the rabbit carotid artery to testosterone by a mechanism that at least includes an increased modulatory activity of the endothelial nitric oxide and the shift of the prostanoid balance regulating the relaxant action of testosterone toward the vasodilator prostanoid. Diabetes also reduces the calcium antagonistic actions of testosterone, which may also contribute to its relaxant action.

Partially supported by RETICS-RENEVAS (RD06/0026/0006) from ISCIII.