Acetylcholine output and foetal vascular resistance of human perfused placental cotyleda

1 The foetal villous vessels of single cotyleda of human placentae have been perfused with a constant flow of Krebs solution, recording inflow pressure and passing the venous perfusate in cascade over guinea‐pig ileum and rat stomach strip preparations in vitro.2 Each cotyledon released for at least 4 h a substance that was probably acetylcholine. The perfusate caused contractions of both preparations which were inhibited by atropine or hyoscine and potentiated by physostigmine. Contractile activity was destroyed after incubation at 37°C of perfusate with acetylcholinesterase but not with acetylcholinesterase plus physostigmine. 3 When the perfusion temperature was lowered to 34°C or below, acetylcholine output was reduced, the extent depending on the fall in temperature. 4 No change in resistance of the villous vessels occurred during the changes in temperature or in the presence at 37°C of atropine, hyoscine, hexamethonium, (+)‐tubocurarine, hemicholinium‐3 or bretylium. 5 Submaximal vasoconstrictor responses of the villous vessels to the thromboxane A 2 ‐mimetic U46619 were not affected by reduction of the perfusion temperature to 30°C, which lowered acetylcholine‐like output by approximately 70%. Responses to U46619, at 37°C, were unchanged during the presence of atropine or hyoscine. 6 Acetylcholine is released into the foetal circulation of the human placenta but no evidence could be obtained that it affects villous vascular smooth muscle tone or vasoconstrictor responses.