The receptors mediating the contractions to both exogenously applied noradrenaline and electrical field stimulation (EFS) were characterized in horse isolated penile resistance arteries. The alpha 1-adrenoceptor-selective antagonist, prazosin, caused competitive rightward shifts of the contractile concentration-response curves (CRC) to phenylephrine. The alpha 2-antagonist, rauwolscine, also displaced to the right the CRC to the alpha 2-adrenoceptor-selective agonist, BHT 920. EFS (0.3 ms, 20-second trains) caused tetrodotoxin-sensitive frequency-dependent contractions which were enhanced in the presence of NG-nitro-L-arginine (L-NOARG, 3 x 10(-5) M), but not affected by mechanical endothelial cell removal. In experiments performed in the presence of L-NOARG, prazosin inhibited contractions to EFS, while rauwolscine inconsistently enhanced the contractile responses. Exogenously added noradrenaline induced contractions which were not changed in endothelium-denuded arteries, but significantly increased in the presence of L-NOARG. Prazosin inhibited the noradrenaline-induced contractions, while rauwolscine did not change the response to noradrenaline either alone or in the presence of prazosin. In the presence of phentolamine (10(-5) M), isoprenaline, adrenaline and the beta 2-adrenoceptor agonist, salbutamol, concentration-dependently relaxed penile resistance arteries, while the relaxations to noradrenaline and dobutamine, which activate beta 1-adrenoceptors, were negligible. Isoprenaline-induced relaxations were not changed in the presence of the beta 1-antagonist, atenolol (10(-7)-10(-6) M), but competitively inhibited by the beta 2-adrenoceptor antagonist, butoxamine (10(-6)-10(-5) M). The present results indicate that stimulation of adrenergic nerves in horse penile resistance arteries releases noradrenaline, which induces vasoconstriction through a predominant activation of alpha 1-adrenoceptors, while postjunctional alpha 2-adrenoceptors apparently play a minor role. Functional beta 2-adrenoceptors are also present in these arteries.