Slow‐reacting substance produced in anaphylaxis (SRS‐A) increased resistance of the lungs to inflation in the guinea‐pig in vivo and caused isolated preparations of its tracheobronchial muscle to contract. SRS‐A also contracted human isolated bronchial muscle and some but not all preparations of rabbit trachea. Nonsteroid anti‐inflammatory drugs, which antagonize bronchoconstriction induced by kinins, but not that by histamine, acetylcholine, 5‐hydroxytryptamine, substance P, angiotensin or lung prostaglandin, also antagonized the bronchoconstrictor action of SRS‐A. This antagonism resembled that of kinins in being surmounted by higher doses of agonist, in the potencies of active drugs and in the types of drugs which were inactive. However, receptors in guinea‐pig tracheobronchial muscle for SRS‐A seem to be distinct from those for bradykinin, since preparations of this muscle could become unresponsive to either agent in vivo and in vitro, while remaining responsive to the other.

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