Although estrogens have been to be vasoactive hormones, the vascular effects
of testosterone are not well defined. Also, administration of testosterone to men with angina
has been shown to reduce myocardial ischemia. The mechanism of this effect is not clear
but could be via an influence on coronary artery tone. We therefore planned this study to
examine the vascular effects of testosterone in-vitro on the coronary artery strips and the
potential mechanisms of its action. Strips of coronary artery were obtained from Adult male
Newzea land white rabbits and mounted in Krebs solution in 50 ml organ chambers at
37oC. These strips are exposed to PGF2α as a vasoconstrictive substance then testosterone is added alone and these experiments are repeated in strips pre-incubated with different
agents. Testosterone induces a significant relaxation of rabbit coronary artery strips precontracted by PGF2α. Incubation of coronary strips with N-nitro-L-arginine methyl ester
(L-NAME) inhibits partially the relaxing effect of T. However, incubation of these strips with
indomethacin did not affect the relaxing effect of T. Moreover, incubation with barium
chloride, the relaxing response of T was significantly attenuated. In conclusion, testosterone
causes vasodilatation in coronary artery and the mechanism of this response involved the
release of nitric oxide from endothelium and the stimulation of voltage dependent K channels
is responsible, at least in part, for the testosterone-induced relaxation of rabbit coronary
arteries. This effect may be one of the explanations as to why testosterone has previously
been shown to demonstrate beneficial effects on anginal symptoms.

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