Adrenoceptor-mediated regulation of the contractility in horse penile resistance arteries

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 N-G-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-NOARC. 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 Pz-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 Pt-adrenoceptor antagonist, butoxamine (10(-6)-10(-5) M). The present results indicate that stimulation of adrenergic nerves in horse penile resistance arteries releases noradenaline, 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.