The effect of adrenaline, noradrenaline, and isoprenaline was studiedin vitroon the spirally‐cut trachea and in anaesthetized animalsin vivo. In thein vitrostudies, all agents caused a relaxation of the tracheal muscles, and the relative potencies were in descending order, isoprenaline (142.2), adrenaline (21.9), and noradrenaline (1.0). After pretreatment for 20 minutes with propranolol (>0.5 μg/ml) or INPEA (>3 μg/ml) adrenaline and noradrenaline caused a contraction of the tracheal muscles. The effect of noradrenaline was 0.44 times that of adrenaline. The constrictor effect of adrenaline and noradrenaline was antagonized or completely inhibited by the α‐receptor blocking agents phenoxy‐benzamine and dibenamine in a concentration of 1–5 μg/ml. Isoprenaline did not produce any contraction of the tracheal muscles after pretreatment with propranolol or INPEA. In thein vivostudies, the animals were anaesthetized with pentobarbital sodium (50 mg/kg intraperitoneally). Intravenous injections were made into the right jugular vein. Changes in tidal volume were recorded according to the method of KONZETT&RÖSSLER. Adrenaline, in the doses 2–4 μg/kg, produced a weak bronchoconstriction that was enhanced after pretreatment of the animals with propranolol (2 mg/kg). The bronchoconstrictor effect of adrenaline and noradrenaline was not affected by atropine but was inhibited by phenoxybenzamine or dibenamine (1–2 mg/kg). Isoprenaline in doses up to 0.1 mg/kg did not produce any bronchoconstriction after pretreatment with propranolol. The results obtained suggest that the smooth muscles in the guinea‐pig trachea and lung contain both α‐ and β‐receptors, the