PGE(2) INHIBITS ACETYLCHOLINE-RELEASE FROM CHOLINERGIC NERVES IN CANINE BUT NOT EQUINE AIRWAYS

The effects of exogenous prostaglandin E(2) (PGE(2)) and endogenous pr ostanoids on cholinergic neurotransmission were determined by measurem ent of acetylcholine (ACh) release from canine and equine airway tissu es. Trachealis strips and bronchial segments were suspended in 2 ml ti ssue baths. ACh release was induced by electrical field stimulation (E FS), and its content in tissue bath liquid was measured by high pressu re liquid chromatography (HPLC) with electrochemical detection. In can ine airways, exogenous PGE(2) (10(-9) to 10(-7) M) inhibited ACh relea se concentration-dependently, whereas inhibition of endogenous prostan oid production by indomethacin (3 x 10(-6) M) augmented ACh release. B y contrast, in equine airways, exogenous PGE(2) had no effect on ACh r elease in bronchi but at 10(-7) M augmented ACh release in the trachea . Cyclooxygenase inhibition by either indomethacin or meclofenamate (1 0(-6) M) did not influence ACh release. We conclude that exogenous PGE (2) and endogenous prostanoids inhibit ACh release from cholinergic ne rves in canine but not equine airways.