Relation between density (maximum binding) of alpha adrenoceptor binding sites and contractile response in four canine vascular tissues.

In microsomal fractions from dog aorta, saphenous veins, mesenteric arteries and veins, both [3H]prazosin and [3H]rauwolscine displayed monophasic saturation in binding. The Kd for [3H] rauwolscine binding was similar for all these blood vessels, but the maximum number of [3H]rauwolscine binding sites was 3 to 7 times higher in veins compared to arteries. The Kd for [3H] prazosin was higher in saphenous vein than that in the arteries. The maximum number of binding sites for [3H]prazosin was similar, except for that in aorta, which was 3 times greater. Phenylephrine (alpha-1 adrenoceptor selective agonist) or norepinephrine (nonselective adrenoceptor agonist) produced similar maximal responses in all vessels. The alpha-2 adrenoceptor selective agonist, B-HT 920 (2-amino-6-allyl-3,4,7,8-tetrahydro-6H-thiazolo[5,4-d]-azepine)-induced contraction in veins but not in arteries. Prazosin (10(-6) M) inhibited completely the contractions to norepinephrine (3 x 10(-6) M) in mesenteric arteries and to phenylephrine (3 x 10(-6) M) in arteries and veins. Contractile responses of mesenteric artery were unaffected by rauwolscine. Rauwolscine (10(-7) M) caused a greater parallel rightward shift of the concentration-response curve to norepinephrine than did prazosin (10(-7) M) in saphenous veins, and a further rightward shift of responses to norepinephrine after 10(-7) M prazosin in mesenteric vein and saphenous vein and abolished B-HT 920-induced responses at alpha-2 adrenoceptors. The tissues responding to B-HT-920 correspond to those having the highest alpha-2 receptor density as measured by [3H]rauwolscine binding. The density of such sites required for contraction to be initiated in veins was much higher than with alpha-1 adrenoceptor sites.(ABSTRACT TRUNCATED AT 250 WORDS)