Alpha-1 adrenergic receptors were examined in rat caudal artery using radioligand binding of [125I]labeled BE 2254 (125IBE) and in vitro contraction measurements. 125IBE bound rapidly and reversibly to a single class of high affinity binding sites in membrane preparations of caudal artery. Scatchard analysis gave an equilibrium dissociation constant (KD) of 110 pM and a density of binding sites of 115 fmol/mg of protein. Antagonists inhibited 125IBE binding and phenylephrine-induced contractions competitively, with an order of potency of prazosin greater than ARC 239 greater than phentolamine greater than yohimbine. pA2 values for inhibition of phenylephrine-induced contraction correlated well with KD values for inhibition of specific 125IBE binding. A number of other full and partial agonists also caused contraction of caudal arteries with an order of potency of epinephrine greater than norepinephrine greater than phenylephrine greater than methoxamine. The order of potency of agonists and the potencies of antagonists suggests that the contractile responses of rat caudal artery were mediated by alpha-1 adrenergic receptors. The EC50 values of partial agonists in causing contraction correlated well with their KD values for inhibition of specific 125IBE binding. However, the EC50 values for full agonists were 30 to 200 times lower than their KD values. Treatment of caudal arteries in vitro with 0.1 microM phenoxybenzamine for 10 min to inactivate alpha adrenergic receptors decreased both the potency of full agonists in causing contraction and the maximal contractile response.(ABSTRACT TRUNCATED AT 250 WORDS)