Please use this identifier to cite or link to this item: https://ahro.austin.org.au/austinjspui/handle/1/10183
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dc.contributor.authorSartor, Daniela Men
dc.contributor.authorVerberne, Anthony J Men
dc.date.accessioned2015-05-15T23:33:12Z
dc.date.available2015-05-15T23:33:12Z
dc.date.issued2006-06-22en
dc.identifier.citationAmerican Journal of Physiology. Regulatory, Integrative and Comparative Physiology 2006; 291(5): R1390-8en
dc.identifier.govdoc16793934en
dc.identifier.otherPUBMEDen
dc.identifier.urihttp://ahro.austin.org.au/austinjspui/handle/1/10183en
dc.description.abstractThe gastrointestinal hormone CCK inhibits a subset of presympathetic neurons in the rostroventrolateral medulla (RVLM) that may be responsible for driving the sympathetic vasomotor outflow to the gastrointestinal circulation. We tested the hypothesis that the central neurocircuitry of this novel sympathoinhibitory reflex involves a relay in the caudal ventrolateral medullary (CVLM) depressor area. Blood pressure and greater splanchnic sympathetic nerve discharge (SSND) or lumbar sympathetic nerve discharge (LSND) were monitored in anesthetised, paralyzed male Sprague-Dawley rats. The effects of phenylephrine (PE, 10 microg/kg iv; baroreflex activation), phenylbiguanide (PBG, 10 microg/kg iv; von Bezold-Jarisch reflex) and CCK (4 or 8 microg/kg iv) on SSND or LSND, were tested before and after bilateral injection of 50-100 nl of the GABAA agonist muscimol (1.75 mM; n=6, SSND; n=7, LSND) or the excitatory amino acid antagonist kynurenate (55 mM; n=7, SSND) into the CVLM. PE and PBG elicited splanchnic and lumbar sympathoinhibitory responses that were abolished by bilateral muscimol or kynurenate injection into the CVLM. Similarly, the inhibitory effect of CCK on SSND was abolished after neuronal inhibition within the CVLM. In contrast, CCK-evoked lumbar sympathoexcitation was accentuated following bilateral CVLM inhibition. In control experiments (n=7), these agents were injected outside the CVLM and had no effect on splanchnic sympathoinhibitory responses to PE, PBG, and CCK. In conclusion, neurons in the CVLM are necessary for the splanchnic but not lumbar sympathetic vasomotor reflex response to CCK. This strengthens the view that subpopulations of RVLM neurons supply sympathetic vasomotor outflow to specific vascular territories.en
dc.language.isoenen
dc.subject.otherAdrenergic alpha-Agonists.pharmacologyen
dc.subject.otherAnimalsen
dc.subject.otherBiguanides.pharmacologyen
dc.subject.otherCholagogues and Choleretics.pharmacologyen
dc.subject.otherCholecystokinin.pharmacologyen
dc.subject.otherExcitatory Amino Acid Antagonists.pharmacologyen
dc.subject.otherGABA Agonists.pharmacologyen
dc.subject.otherKynurenic Acid.pharmacologyen
dc.subject.otherLumbosacral Plexus.drug effects.physiologyen
dc.subject.otherMaleen
dc.subject.otherMedulla Oblongata.drug effects.physiologyen
dc.subject.otherMuscimol.pharmacologyen
dc.subject.otherNeurons.drug effects.physiologyen
dc.subject.otherPhenylephrine.pharmacologyen
dc.subject.otherRatsen
dc.subject.otherRats, Sprague-Dawleyen
dc.subject.otherSerotonin Receptor Agonists.pharmacologyen
dc.subject.otherSplanchnic Nerves.drug effects.physiologyen
dc.subject.otherSympathetic Nervous System.drug effects.physiologyen
dc.subject.otherSynaptic Transmission.drug effects.physiologyen
dc.titleThe sympathoinhibitory effects of systemic cholecystokinin are dependent on neurons in the caudal ventrolateral medulla in the rat.en
dc.typeJournal Articleen
dc.identifier.journaltitleAmerican journal of physiology. Regulatory, integrative and comparative physiologyen
dc.identifier.affiliationUniversity of Melbourne, Clinical Pharmacology and Therapeutics Unit, Dept. of Medicine, Austin Health, Heidelberg, Victoria 3084, Australiaen
dc.identifier.doi10.1152/ajpregu.00314.2006en
dc.description.pagesR1390-8en
dc.relation.urlhttps://pubmed.ncbi.nlm.nih.gov/16793934en
dc.type.austinJournal Articleen
item.openairetypeJournal Article-
item.fulltextNo Fulltext-
item.languageiso639-1en-
item.openairecristypehttp://purl.org/coar/resource_type/c_18cf-
item.grantfulltextnone-
item.cerifentitytypePublications-
crisitem.author.deptClinical Pharmacology and Therapeutics-
crisitem.author.deptMedicine (University of Melbourne)-
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