Recent studies have shown that testosterone
induces relaxation of different arteries, although the mechanism
of this action is still under debate. We investigated
the involvement of potassium channels in this mechanism.
Using standard organ bath techniques, rings of human
umbilical arteries (HUA) without endothelium were contracted
by serotonin (5-HT, 1 μM), histamine (10 μM) and
potassium chloride (KCl, 30 and 60 mM), and the
vasorelaxant effect of testosterone was analysed. Testosterone
(100 μM) relaxed human umbilical arteries contracted
with 5-HT (30.1±3.2%), histamine (55.1±2.6%), KCl
30 mM (52.9±8.3%) and KCl 60 mM (54.8±6.3%).
Flutamide (10 μM), an inhibitor of classical intracellular
testosterone receptor, and glibenclamide, an ATP-sensitive
potassium-channels (KATP) inhibitor, did not influence the
testosterone relaxant effect. 4-aminopyridine, a voltagesensitive
potassium-channels (Kv) inhibitor, decreased the
effect of testosterone on histamine- and 5-HT-contracted
arteries. Tetraethylammonium (TEA), which inhibits Kv
channels and large-conductance Ca2+-activated potassium
channels (BKCa), decreased the effect of testosterone on
KCl (60 mM)-contracted and 5-HT-contracted HUA. In
conclusion, testosterone induces relaxation of HUA, and
this effect does not appear to be mediated via a classic intracellular testosterone receptor-dependent mechanism.
Our results suggest that this relaxation is partially mediated
by activation of BKCa and KV channels. The involvement
of these two channels in testosterone-relaxant mechanism is
dependent on the pathways activated by the contractile
agent used
