Human resistance arteries (144-332-mu-m diam) from colon, pericardial fat, and skeletal muscle were mounted in a myograph for measurements of isometric contractions under conditions of partial depolarization by potassium chloride. In all preparations, both phenylephrine (alpha-1-selective agonist) and B-HT 933 (alpha-2-selective agonist) evoked concentration-dependent contractions that were antagonized by the alpha-1-selective antagonist prazosin (10(-8) M) and the alpha-2-selective antagonist yohimbine (10(-7) M), respectively. The affinities (expressed as pK(B) values) of prazosin for the receptor mediating the responses to phenylephrine were 8.88-9.41, whereas the affinities of yohimbine for the receptor mediating the responses to B-HT 933 were 7.71-7.97. Norepinephrine (mixed alpha-1-agonist/alpha-2-agonist) also elicited concentration-dependent responses that were modestly, but significantly, antagonized by prazosin alone and yohimbine alone at the above-mentioned concentrations. The two antagonists in combination, however, effectively antagonized the responses to this agonist. These findings strongly suggest the presence of functional, postjunctional alpha-1- and alpha-2-adrenoceptors in isolated human resistance arteries from colon, pericardial fat, and skeletal muscle and that responses to norepinephrine in these vessels are mediated by both alpha-adrenoceptor subtypes.