Inhibitory effects of prostaglandin E1 and E2 on cholinergic transmission in isolated canine tracheal muscle.
The contractile response of the isolated canine tracheal muscle to the transmural nerve stimulation was depressed by atropine and augmented by physostigmine, indicating that the response was predominantly mediated via the parasympathetic nerve. The contractile response to the transmural nerve stimulation was inhibited by prostaglandin E1 (PGE1) and E2 (PGE2) (10(-7) to 10(-5) g/ml) and the inhibitory action of PGE1 was more potent than that of PGE2. On the other hand, the contractile response of the tracheal muscle to exogenously administered ACh was unaffected by 10(-6) g/ml of PGE1 and PGE2. These findings lend support to the hypothesis that the PGE series, in a manner similar to adrenergic transmission, are involved in a negative feed-back control mechanism for the transmitter release in cholinergic transmission.
D000109:Acetylcholine / Q000494:pharmacology; D000818:Animals; D001285:Atropine / Q000494:pharmacology; D004285:Dogs; D004347:Drug Interactions; D004558:Electric Stimulation; D005260:Female; D066298:In Vitro Techniques; D008297:Male; D009119:Muscle Contraction / Q000187:drug effects; D009132:Muscles / Q000294:innervation* / Q000502:physiology; D010275:Parasympathetic Nervous System / Q000187:drug effects*; D010830:Physostigmine / Q000494:pharmacology; D011458:Prostaglandins E / Q000494:pharmacology*; D009435:Synaptic Transmission / Q000187:drug effects*; D014043:Tolazoline / Q000494:pharmacology; D014132:Trachea / Q000294:innervation* / Q000502:physiology
D011458:Prostaglandins E; D001285:Atropine; D010830:Physostigmine; D014043:Tolazoline; D000109:Acetylcholine