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Mechanism of the noradrenergic motor control on the lower oesophageal sphincter in the cat.
Author(s) -
Gonella J,
Niel J P,
Roman C
Publication year - 1980
Publication title -
the journal of physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.802
H-Index - 240
eISSN - 1469-7793
pISSN - 0022-3751
DOI - 10.1113/jphysiol.1980.sp013395
Subject(s) - acetylcholine , tetrodotoxin , choline , endocrinology , medicine , atropine , depolarization , chemistry , cholinergic , neurotransmitter , biology , central nervous system
1. The release of labelled acetylcholine has been measured on lower oesophageal sphincter (l.o.s.) muscular strips previously loaded with tritiated choline. 2. This release was greatly increased by noradrenaline 10(‐5) g/ml. and unaffected by atropine 10(‐6) g/ml., but it was practically abolished if hemicholinium 5.2 X 10(‐4) M was added to the incubating bath containing the tritiated choline. 3. A radioautographic study of sections of l.o.s. strips loaded with tritiated choline showed that the radioactivity was mainly located in the nervous cells of the enteric plexuses and that the muscular cells were very poorly labelled. 4. The increased release of acetylcholine induced by noradrenaline did not occur in a Ca2+‐free or in a hypermagnesic Tyrode (12 mM). 5. Tetrodotoxin 10(‐6) G/ml. had no effect on the increased release of acetylcholine induced by noradrenaline. In addition, sucrose gap recordings showed that the depolarizing effect of noradrenaline on l.o.s. muscular strips was unaffected by tetrodotoxin 10(‐6) g/ml. 6. It is concluded that acetylcholine released in the l.o.s. under the action of noradrenaline originated from the synaptic endings of the cholinergic intramural neurones.