ADRENOCEPTOR-MEDIATED REGULATION OF THE CONTRACTILITY IN HORSE PENILERESISTANCE ARTERIES

Citation
U. Simonsen et al., ADRENOCEPTOR-MEDIATED REGULATION OF THE CONTRACTILITY IN HORSE PENILERESISTANCE ARTERIES, Journal of vascular research, 34(2), 1997, pp. 90-102
Citations number
45
Categorie Soggetti
Peripheal Vascular Diseas",Physiology
ISSN journal
10181172
Volume
34
Issue
2
Year of publication
1997
Pages
90 - 102
Database
ISI
SICI code
1018-1172(1997)34:2<90:AROTCI>2.0.ZU;2-3
Abstract
The receptors mediating the contractions to both exogenously applied n oradrenaline and electrical field stimulation (EFS) were characterized in horse isolated penile resistance arteries. The alpha(1)-adrenocept or-selective antagonist, prazosin, caused competitive rightward shifts of the contractile concentration-response curves (CRC) to phenylephri ne. 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-depe ndent 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 endoth elial cell removal. In experiments performed in the presence of L-NOAR G, prazosin inhibited contractions to EFS, while rauwolscine inconsist ently enhanced the contractile responses. Exogenously added noradrenal ine induced contractions which were not changed in endothelium-denuded arteries, but significantly increased in the presence of L-NOARC. Pra zosin inhibited the noradrenaline-induced contractions, while rauwolsc ine did not change the response to noradrenaline either alone or in th e presence of prazosin. In the presence of phentolamine (10(-5) M), is oprenaline, adrenaline and the Pz-adrenoceptor agonist, salbutamol, co ncentration-dependently relaxed penile resistance arteries, while the relaxations to noradrenaline and dobutamine, which activate beta(1)-ad renoceptors, were negligible. Isoprenaline-induced relaxations were no t changed in the presence of the beta(1)-antagonist, atenolol ( 10(-7) -10(-6) M), but competitively inhibited by the Pt-adrenoceptor antagon ist, butoxamine (10(-6)-10(-5) M). The present results indicate that s timulation of adrenergic nerves in horse penile resistance arteries re leases noradenaline, which induces vasoconstriction through a predomin ant activation of alpha(1)-adrenoceptors, while postjunctional alpha(2 )-adrenoceptors apparently play a minor role. Functional beta(2)-adren oceptors are also present in these arteries.