1985
DOI: 10.1016/0014-2999(85)90051-2
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Influence of peripheral and central administration of apomorphine and morphine on intragastric pressure in the dog

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Cited by 7 publications
(2 citation statements)
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“…Thus when gastric filling occurs, the corpus fills without a n undue rise in intragastric pressure. Additional corpus relaxation, for example as evoked by feedback from the duodenum during gastric emptying (17) or as part of the prodromal visceral response of emesis (18), imparts fine control over the gastric reservoir function, enabling gastric contents to be retained in the proximal stomach as a means of delaying the aboral progression of chyme. Such responses are likely to come about via concomitant changes in the level of discharge in the cholinergic and NANC vagal pathways, which in turn modifies the gain of the local enteric circuits.…”
Section: Discussionmentioning
confidence: 99%
“…Thus when gastric filling occurs, the corpus fills without a n undue rise in intragastric pressure. Additional corpus relaxation, for example as evoked by feedback from the duodenum during gastric emptying (17) or as part of the prodromal visceral response of emesis (18), imparts fine control over the gastric reservoir function, enabling gastric contents to be retained in the proximal stomach as a means of delaying the aboral progression of chyme. Such responses are likely to come about via concomitant changes in the level of discharge in the cholinergic and NANC vagal pathways, which in turn modifies the gain of the local enteric circuits.…”
Section: Discussionmentioning
confidence: 99%
“…For instance, intravenous administration of apomorphine, that is a nonspecific dopaminergic agonist and induces emesis, evokes two distinct gastric motor responses in rat. One is the inhibition of phasic contractions that appear just after administration (Abrahamsson et al, 1973;Blancquaert et al, 1985), and the other is an increase in the frequency of small phasic contractions accompanied by increased gastric tone appearing with a relatively longer delay (Koga et al, 2003). Nicotine is also known to induce excitatory and inhibitory effects on the gastrointestinal tract, some of which may be caused by interaction of nicotine with nAChR in the medullla oblongata (Nagata and Osumi, 1991;Ferreira et al, 2000Ferreira et al, , 2001.…”
Section: Discussionmentioning
confidence: 99%