Abstract. To determine whether functional atypical -adrenoceptors (3-adrenoceptors) are present in pulmonary vascular smooth muscle, we studied isolated canine pulmonary arterial rings under isometric conditions in vitro. Addition of -adrenoceptor agonists produced a concentration-dependent relaxation of noradrenaline-precontracted tissues, a rank order potency being isoproterenol (1) salbutamol (0.95) selective 3-adrenoceptor agonists, CL 316243 (0.85), and BRL 37344 (0.83). A marked desensitization to salbutamol occurred by pretreatment with salbutamol but not with CL 316243. When 1-adrenoceptors had been blocked, the relaxant responses to salbutamol were competitively antagonized by the 2-adrenoceptor antagonist ICI 118551 with a pA2 value of 7.67 0.21 (mean S.E.), but the response to CL 316243 was weekly antagonized by ICI 118551 only at a high concentration of 105 M, where an apparent pA2 value was 5.24. In contrast, cyanopindolol, a nonselective -adrenoceptor antagonist, antagonized CL 316243induced relaxation in a competitive manner with a pA2 of 6.10 0.11. This pA2 value was lower than that when salbutamol was used as an agonist (6.69 0.14, p 0.01). Intracellular 3,5-cyclic adenosine monophosphate (cAMP) levels were increased by CL 316243 in a concentration-dependent fashion, an effect that was not altered by ICI 118551. These results suggest that 3-adrenoceptors may exist in canine pulmonary artery smooth muscle and that stimulation of this atypical receptor causes vasodilation through a cAMP-dependent pathway.