Organ chamber experiments were designed to determine the effects of anisodamine, an alkaloid structurally related to atropine, on prejunctional M2- and postjunctional M2-muscarinic receptors in isolated canine saphenous veins. The results showed that both acetylcholine-induced contraction and dilatation were inhibited in a competitive manner by anisodamine or atropine. The affinity of anisodamine for pre- and postjunctional muscarinic receptors was comparable (pKB = 7.78 and 7.86, respectively). However, compared with atropine, the affinity of anisodamine for prejunctional M2-receptors was about 1/8; while that for postjunctional M1-receptors was only 1/25 of that of atropine (pKB = 8.69 and 9.25, respectively for atropine). The data demonstrate that anisodamine is a non-selective muscarinic antagonist, a modulator rather than a vasodilator. The probable mechanisms involved are discussed.