Please use this identifier to cite or link to this item: https://ahro.austin.org.au/austinjspui/handle/1/10011
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dc.contributor.authorSartor, Daniela Men
dc.contributor.authorShulkes, Arthuren
dc.contributor.authorVerberne, Anthony J Men
dc.date.accessioned2015-05-15T23:19:23Z
dc.date.available2015-05-15T23:19:23Z
dc.date.issued2005-10-20en
dc.identifier.citationAmerican Journal of Physiology. Regulatory, Integrative and Comparative Physiology 2005; 290(3): R625-33en
dc.identifier.govdoc16239368en
dc.identifier.otherPUBMEDen
dc.identifier.urihttp://ahro.austin.org.au/austinjspui/handle/1/10011en
dc.description.abstractIngestion of a meal results in gastrointestinal (GI) hyperemia and is associated with systemic and paracrine release of a number of peptide hormones, including cholecystokinin (CCK) and 5-hydroxytryptamine (5-HT). Systemic administration of CCK octapeptide inhibits a subset of presympathetic neurons of the rostroventrolateral medulla (RVLM) that may be responsible for driving the sympathetic vasomotor tone to the GI viscera. The aim of this study was to determine whether endogenous release of CCK and/or 5-HT also inhibits CCK-sensitive RVLM neurons. The effects of intraduodenal administration of the secretagogues sodium oleate (SO) and soybean trypsin inhibitor (SBTI) on circulating levels of CCK and 5-HT were examined. In separate experiments, the discharge rates of barosensitive, medullospinal, CCK-sensitive RVLM presympathetic vasomotor neurons were recorded after rapid intraduodenal infusion of SO-SBTI or water. Alternatively, animals were pretreated with the CCK1 receptor antagonists devazepide and lorglumide or the 5-HT3 antagonist MDL-72222 before SO-SBTI administration. Secretagogue infusion significantly increased the level of circulating CCK, but not 5-HT. SO-SBTI significantly decreased (58%) the neuronal firing rate of CCK-sensitive RVLM neurons compared with water (5%). CCK1 receptor antagonists did not reverse SO-SBTI-induced neuronal inhibition (58%), whereas the 5-HT3 antagonist significantly attenuated the effect (22%). This study demonstrates a functional relation between a subset of RVLM presympathetic vasomotor neurons and meal-related signals arising from the GI tract. It is likely that endogenously released 5-HT acts in a paracrine fashion on GI 5-HT3 receptors to initiate reflex inhibition of these neurons, resulting in GI vasodilatation by withdrawal of sympathetic tone.en
dc.language.isoenen
dc.subject.otherAnimalsen
dc.subject.otherCholecystokinin.metabolismen
dc.subject.otherGastrointestinal Tract.physiologyen
dc.subject.otherIntestines.innervation.physiologyen
dc.subject.otherMaleen
dc.subject.otherMotor Neurons.physiologyen
dc.subject.otherRatsen
dc.subject.otherRats, Sprague-Dawleyen
dc.subject.otherSerotonin.metabolismen
dc.subject.otherSignal Transduction.physiologyen
dc.subject.otherSpinal Cord.physiologyen
dc.subject.otherSympathetic Nervous System.physiologyen
dc.subject.otherVasomotor System.physiologyen
dc.titleAn enteric signal regulates putative gastrointestinal presympathetic vasomotor neurons in rats.en
dc.typeJournal Articleen
dc.identifier.journaltitleAmerican journal of physiology. Regulatory, integrative and comparative physiologyen
dc.identifier.affiliationClinical Pharmacology and Therapeutics Unit, Department of Medicine, University of Melbourne, Austin Health, Heidelberg, Victoria 3084, Australiaen
dc.identifier.doi10.1152/ajpregu.00639.2005en
dc.description.pagesR625-33en
dc.relation.urlhttps://pubmed.ncbi.nlm.nih.gov/16239368en
dc.type.austinJournal Articleen
item.openairecristypehttp://purl.org/coar/resource_type/c_18cf-
item.fulltextNo Fulltext-
item.cerifentitytypePublications-
item.grantfulltextnone-
item.languageiso639-1en-
item.openairetypeJournal Article-
crisitem.author.deptClinical Pharmacology and Therapeutics-
crisitem.author.deptMedicine (University of Melbourne)-
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