The adrenergic contractile responses of smooth muscles in the vascular wall of guinea pig pulmonary arteries were studied during ovalbumin sensitization. Sensitization was followed by inhibition of contractile responses to an alpha-adrenoceptor agonist mesatone, prevented endothelium-derived relaxation, and potentiated the contractile response to isoproterenol. Administration of a beta-adrenoceptor agonist isoproterenol potentiated the increase in mechanical strain of smooth muscles in the pulmonary artery precontracted with high-potassium Krebs solution. Removal of the endothelium had no effect on the contractile response of smooth muscle segments from the pulmonary artery of intact and sensitized guinea pigs to b-adrenergic influences. The contractile responses of smooth muscles of the pulmonary artery are associated with activity of the cAMP-dependent signal system and play a role in the pathogenesis of ventilation-perfusion disturbances during atopic inflammation.