U. Simonsen et al., ADRENOCEPTOR-MEDIATED REGULATION OF THE CONTRACTILITY IN HORSE PENILERESISTANCE ARTERIES, Journal of vascular research, 34(2), 1997, pp. 90-102
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.