The postjunctional alpha-adrenoceptors in human long saphenous vein were characterized using alpha-adrenoceptor subtype selective agonists and antagonists. The order of potency for the alpha-adrenoceptor agonists used was: Clonidine (alpha 2) greater than BHT-920 (alpha 2) greater than naphazoline (alpha 2) greater than guanfacine (alpha 2) greater than cirazoline (alpha 1) greater than phenylephrine (alpha 1) greater than ST 587 (alpha 1) greater than BHT-933 (alpha 2). Clonidine had the same potency as noradrenaline (NA), but was 52 times more potent than phenylephrine (pEC50 7.09 and 5.37, respectively). Phenylephrine and guanfacine had intrinsic activities that did not differ from that of NA, whereas the intrinsic activities of the other agonists were significantly lower. The highly selective alpha 1-adrenoceptor antagonist prazosin in concentrations 10(-9)-10(-7) M was unable to cause a significant shift of the NA concentration response (cr) curve to the right. However, the alpha 2-adrenoceptor antagonists yohimbine and rauwolscine in concentrations 10(-8)-10(-6) M shifted the NA cr-curve towards higher concentrations. No concentration of any antagonist used significantly attenuated the maximum contraction. The slope of the regression line in the Schild plot differed significantly from unity for rauwolscine but not for yohimbine, and the pA2-values were 9.00 and 8.27, respectively. These results suggest that the contraction mediating alpha-adrenoceptors in the human saphenous vein are mainly of the alpha 2-type. However, the low slope value of the Schild plot for rauwolscine may indicate the presence of a small population of alpha 1-adrenoceptors.