A possible mechanism of airway hyperresponsiveness induced by prostaglandin F2 alpha and thromboxane A2.

Abstract

To elucidate the precise mechanisms of airway hyperresponsiveness induced by prostaglandin F2 alpha (PGF2 alpha) and thromboxane A2 (TXA2), we investigated the effects of the subthreshold dose (the highest dose which does not lead to contraction) of PGF2 alpha and stable TXA2 analogue, STA2 (epithiomethano-TXA2), on the smooth muscle contraction evoked by acetylcholine (ACh) and electrical field stimulation (EFS) in the canine trachea. These prostanoids produced no changes in the contractile response to both these stimuli. Thus, neither PGF2 alpha nor TXA2 affect the smooth muscle, as the site of action for ACh is the muscarinic receptor located on smooth muscle. Neither compound affect the postganglionic vagal efferent nerve, because the EFS contracts smooth muscle via activation of the postganglionic vagal efferent neuron. This study, together with our previous observation, suggests that PGF2 alpha and TXA2 induce airway hyperresponsiveness by stimulating vagal sensory endings and by activating the reflex pathway.