Abstract:A pharmacological characterization of the postjunctional α‐adrenoceptors in human superficial epigastric artery and vein was performed, using several α‐adrenoceptor subtype selective agonists, and the antagonists prazosin (α1) and rauwolscine (α22). In the arteries prazosin fulfilled the criteria for a competitive antagonism in concentrations 10‐9‐10‐7M, giving a pA2‐value of 9.17 in the Schild plot. Rauwolscine in concentrations 10‐8‐10‐6M caused less pronounced but significant dextral shifts of the noradrenaline (NA) concentration‐response curves. In the veins rauwolscine behaved like a competitive antagonist (10‐‐10‐6M). The pA2‐value was 9.16. Prazosin 10‐9M displaced the NA concentration‐response curve, but higher concentrations (10‐8and 10‐7M) caused no further displacement. Prazosin reduced the Emax‐values in the veins. In the arteries the rank order of potency for the agonists was: cirazoline (α1)>NA>naphazoline (α2)>guanfacine (α2)>phenylephrine (α1). The intrinsic activities of clonidine (α2), ST 587 (α1), B‐HT 920 (α2) and B‐HT 933 (α2) were too low to allow meaningful comparisons to be made. The rank order of potency in the veins was: NA>clonidine (α2)>naphazoline (α2)>guanfacine (α2)>phenylephrine (α1)>B‐HT 920 (α2)>cirazoline (α1)>B‐HT 933 (α2). The intrinsic activity of ST 587 was low. Only two pEC50‐values could be determined for clonidine in the arteries and these were higher than the pEC50‐values for clonidine in the veins. Phenylephrine, naphazoline and guanfacine were equipotent in both types of vessel. Cirazoline was 135 times more potent and NA was 3 times less potent in the arteries than in the veins. The data suggest that the rank order of potency of subtype selective agonists cannot be used for characterization of the α‐adrenoceptors in human superficial epigastric arteries and veins. Antagonists on the other hand, give distinct satisfactory information. In the arteries α1‐adrenoceptors predominate, but a population of α2‐adrenoceptors cannot be excluded in some patients. In the veins α2‐adrenocep