Experiments were performed on isolated canine and human coronary arteries to study the alpha- and beta-adrenolytic properties of ridazolol. On canine coronary arteries precontracted with prostaglandin F₂ alpha 2 M and pretreated with phentolamine 1 M, ridazolol competitively antagonized the isoproterenol-induced relaxations, with a pA₂ value of 8.5 (7.8–9.1). Thereafter the alpha-adrenolytic activity of ridazolol was assessed on these same canine coronary vessels. Ridazolol activity was compared with that of prazosin on dose-response curves to norepinephrine in the presence of cocaine (30 M) and propranolol (3 M). Schild plots for both drugs gave straight lines, with slopes not different from unity. The pA₂ value was 7.1 (6.8–7.3) for ridazolol and 8.1 (7.9–8.4) for prazosin. In another set of experiments the alpha-adrenolytic activity of ridazolol was compared on canine and human coronary arteries. A submaximal contraction with norepinephrine (10 M) was first assessed in the presence of propranolol 3 M. The addition of ridazolol 3 M significantly decreased the norepinephrine (10 M)-induced contractions of both preparations. However, the inhibition was more pronounced on canine coronary arteries. In conclusion, ridazolol is a potent beta-adrenergic antagonist with moderate alpha-adrenolytic activity. The weaker inhibition of the norepinephrine-induced contraction observed in human preparations suggests the presence of a heteregeneous population of postjunctional alpha adrenoceptors.