Please use this identifier to cite or link to this item: https://ahro.austin.org.au/austinjspui/handle/1/13255
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dc.contributor.authorTrinder, Den
dc.contributor.authorPhillips, P Aen
dc.contributor.authorStephenson, J Men
dc.contributor.authorRisvanis, Johnen
dc.contributor.authorAminian, Aen
dc.contributor.authorAdam, W Ren
dc.contributor.authorCooper, Mark Een
dc.contributor.authorJohnston, Colin Ien
dc.date.accessioned2015-05-16T03:04:31Z
dc.date.available2015-05-16T03:04:31Z
dc.date.issued1994-02-01en
dc.identifier.citationThe American Journal of Physiology; 266(2 Pt 1): E217-23en
dc.identifier.govdoc8141280en
dc.identifier.otherPUBMEDen
dc.identifier.urihttp://ahro.austin.org.au/austinjspui/handle/1/13255en
dc.description.abstractDiabetes mellitus causes hypertonicity, increased plasma arginine vasopressin (AVP), polydipsia, and polyuria. Downregulation of AVP V2 receptors may contribute to the polyuria through diminished V2 receptor-mediated free water retention. After 2 wk of streptozotocin-induced diabetes mellitus, the diabetic rats had raised plasma glucose, AVP, and osmolality levels (P < 0.001) compared with nondiabetic controls (Sham). Insulin treatment (4 U long-acting insulin sc, daily) partially lowered these values (P < 0.01). There was a reduction in the number of renal and hepatic V1 receptors in the diabetic and diabetic+insulin animals compared with the sham animals (P < 0.05). The receptor affinity remained unchanged. In parallel, there was a reduction in maximum AVP-activated total inositol phosphate production in the liver and kidney of the diabetic and diabetic+insulin animals compared with the sham animals (P < 0.05). The density and affinity of renal V2 receptors and AVP-stimulated adenosine 3',5'-cyclic monophosphate production in the diabetic and diabetic+insulin animals were unchanged compared with the sham. These results demonstrate differential regulation of AVP receptors and suggest that downregulation of renal V2 receptors does not contribute to the polyuria of diabetes. In contrast, downregulation of V1 receptors might contribute to diminished V1 receptor-mediated biological responses to AVP seen in diabetes mellitus.en
dc.language.isoenen
dc.subject.otherAnimalsen
dc.subject.otherArginine Vasopressin.pharmacologyen
dc.subject.otherBlood Glucose.metabolismen
dc.subject.otherCyclic AMP.metabolismen
dc.subject.otherDiabetes Mellitus, Experimental.metabolismen
dc.subject.otherDown-Regulationen
dc.subject.otherFemaleen
dc.subject.otherInositol Phosphates.metabolismen
dc.subject.otherInsulin.pharmacologyen
dc.subject.otherKidney.metabolismen
dc.subject.otherRatsen
dc.subject.otherRats, Sprague-Dawleyen
dc.subject.otherReceptors, Vasopressin.metabolismen
dc.subject.otherSecond Messenger Systemsen
dc.titleVasopressin V1 and V2 receptors in diabetes mellitus.en
dc.typeJournal Articleen
dc.identifier.journaltitleAmerican Journal of Physiologyen
dc.identifier.affiliationUniversity of Melbourne, Department of Medicine, Austin Hospital, Heidelberg, Victoria, Australiaen
dc.description.pagesE217-23en
dc.relation.urlhttps://pubmed.ncbi.nlm.nih.gov/8141280en
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-
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