The mechanism of airway hyperresponsiveness (AH) following immediate asthmatic response (IAR) was investigated in ovalbumin (OA)-sensitized guinea-pigs. After IAR, airway responsiveness was significantly increased and propranolol-induced bronchoconstriction (PIB) was so severe that guinea-pigs died. A thromboxane (Tx) synthetase inhibitor CS-518 significantly inhibited AH and PIB, whereas a PAF receptor antagonist WEB-2086 was only slightly effective. These results suggest that TxA2 plays an important role and PAF a partial role in AH following IAR.