Please use this identifier to cite or link to this item: https://ahro.austin.org.au/austinjspui/handle/1/10178
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dc.contributor.authorVerberne, Anthony J Men
dc.contributor.authorMcInerney, Kathleenen
dc.date.accessioned2015-05-15T23:32:48Z
dc.date.available2015-05-15T23:32:48Z
dc.date.issued2006-06-16en
dc.identifier.citationBrain Research 2006; 1102(1): 127-34en
dc.identifier.govdoc16781679en
dc.identifier.otherPUBMEDen
dc.identifier.urihttps://ahro.austin.org.au/austinjspui/handle/1/10178en
dc.description.abstractThe pancreas receives sympathetic input which arises from several premotor cell groups in the CNS including the rostral ventrolateral medulla (RVLM). In this study, we examined the influence of electrical stimulation of the RVLM on pancreatic blood flow measured by laser Doppler flowmetry and gastric blood flow measured by ultrasonic Doppler flowmetry in halothane-anesthetized rats. The laser Doppler flow measurement technique was validated by demonstration that pancreatic conductance was reduced by systemic administration of the vasoconstrictor phenylephrine and increased by the vasodilator sodium nitroprusside. Sympathetic vasomotor withdrawal induced by either administration of phenylbiguanide (2 and 10 microg/kg, i.v.) or electrical stimulation of the central end of the cervical vagal trunk (5 Hz, 2 ms, 50-150 microA) produced depressor responses and increases in pancreatic and gastric vascular conductance. Electrical stimulation of the RVLM (50 Hz, 0.5 ms, 25-75 microA) produced pressor and tachycardic responses accompanied by decreases in pancreatic and gastric vascular conductance. All responses to RVLM stimulation were abolished by blockade of ganglionic neurotransmission (hexamethonium bromide, 20 mg/kg, i.v.). These data suggest that RVLM presympathetic vasomotor neurons are a primary source of tonic sympathetic vasomotor drive to the pancreatic and gastric vasculature.en
dc.language.isoenen
dc.subject.otherAction Potentials.drug effects.radiation effectsen
dc.subject.otherAnalysis of Varianceen
dc.subject.otherAnimalsen
dc.subject.otherBiguanides.pharmacologyen
dc.subject.otherBlood Pressure.drug effects.physiologyen
dc.subject.otherDose-Response Relationship, Radiationen
dc.subject.otherElectric Stimulation.methodsen
dc.subject.otherHeart Rate.drug effects.physiology.radiation effectsen
dc.subject.otherMaleen
dc.subject.otherMedulla Oblongata.cytologyen
dc.subject.otherNeurons.drug effects.physiology.radiation effectsen
dc.subject.otherPancreas.drug effects.physiologyen
dc.subject.otherRatsen
dc.subject.otherRats, Sprague-Dawleyen
dc.subject.otherRegional Blood Flow.drug effects.physiology.radiation effectsen
dc.subject.otherSerotonin Receptor Agonists.pharmacologyen
dc.subject.otherStomach.drug effects.physiology.radiation effectsen
dc.subject.otherVagus Nerve.drug effects.physiology.radiation effectsen
dc.subject.otherVasoconstriction.drug effects.physiologyen
dc.titlePancreatic vasoconstrictor responses are regulated by neurons in the rostral ventrolateral medulla.en
dc.typeJournal Articleen
dc.identifier.journaltitleBrain Researchen
dc.identifier.affiliationDepartment of Medicine, University of Melbourne, Clinical Pharmacology and Therapeutics Unit, Austin Health, Heidelberg Victoria, Australiaen
dc.identifier.doi10.1016/j.brainres.2006.05.031en
dc.description.pages127-34en
dc.relation.urlhttps://pubmed.ncbi.nlm.nih.gov/16781679en
dc.type.austinJournal Articleen
local.name.researcherVerberne, Anthony J M
item.grantfulltextnone-
item.openairetypeJournal Article-
item.languageiso639-1en-
item.fulltextNo Fulltext-
item.openairecristypehttp://purl.org/coar/resource_type/c_18cf-
item.cerifentitytypePublications-
crisitem.author.deptClinical Pharmacology and Therapeutics-
crisitem.author.deptMedicine (University of Melbourne)-
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