Please use this identifier to cite or link to this item: https://ahro.austin.org.au/austinjspui/handle/1/9276
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dc.contributor.authorJandeleit-Dahm, Ken
dc.contributor.authorHannan, K Men
dc.contributor.authorFarrelly, C Aen
dc.contributor.authorAllen, Terri Jen
dc.contributor.authorRumble, J Ren
dc.contributor.authorGilbert, Richard Een
dc.contributor.authorCooper, Mark Een
dc.contributor.authorLittle, P Jen
dc.date.accessioned2015-05-15T22:18:21Z
dc.date.available2015-05-15T22:18:21Z
dc.date.issued2000-12-08en
dc.identifier.citationCirculation Research; 87(12): 1133-40en
dc.identifier.govdoc11110770en
dc.identifier.otherPUBMEDen
dc.identifier.urihttps://ahro.austin.org.au/austinjspui/handle/1/9276en
dc.description.abstractVascular disease often involves vessel hypertrophy with underlying cellular hypertrophy or hyperplasia. Experimental diabetes stimulates hypertrophy of the rat mesenteric vasculature, and we investigated the hypothesis that this hypertrophy is associated with activation of Na(+)-H(+) exchange (NHE) activity. We measured the NHE activity in isolated, intact blood vessels from control and streptozotocin-induced diabetic adult rats using concurrent myography and fluorescence spectroscopy. The role of inhibiting NHE activity in preventing the development of the mesenteric hypertrophy in streptozotocin-diabetic rats was investigated by administration of cariporide (100 mg/kg body weight per day in 3 doses by gavage) after induction of diabetes and subsequently determining vessel weight and structure. The weight of the mesenteric vasculature was not increased 1 week after streptozotocin treatment but was significantly increased by an average of 56% at 3 weeks. NHE activity in mesenteric arteries showed an enhanced maximal velocity (V:(max)) in diabetic vessels at 1 and 3 weeks (0.246+/-0.006 and 0. 238+/-0.007 versus 0.198+/-0.007 pH U/min) with no change in the apparent K:(m). Moreover, NHE-1 mRNA in mesenteric arterioles at 3 weeks after streptozotocin treatment was increased by >60% (55.8+/-6. 4 versus 91.3+/-12.3 fg). Administration of cariporide significantly reduced mesenteric vascular weight, the wall/lumen ratio, and mesenteric extracellular matrix accumulation in the diabetic animals. Our study shows that diabetes in vivo correlates with elevated NHE activity and mRNA in the mesenteric vasculature and furthermore that inhibition of this system prevents the hypertrophic response. These data suggest that NHE may be a target for therapeutic modulation of vascular changes in diabetes.en
dc.language.isoenen
dc.subject.otherAnimalsen
dc.subject.otherAnti-Arrhythmia Agents.pharmacologyen
dc.subject.otherBlood Vesselsen
dc.subject.otherDiabetes Mellitus, Experimental.chemically induced.complications.metabolismen
dc.subject.otherDisease Models, Animalen
dc.subject.otherGuanidines.pharmacologyen
dc.subject.otherHydrogen-Ion Concentrationen
dc.subject.otherHypertrophy.etiology.metabolismen
dc.subject.otherMaleen
dc.subject.otherMesenteric Arteries.drug effects.metabolismen
dc.subject.otherMuscle, Smooth, Vascular.metabolismen
dc.subject.otherRatsen
dc.subject.otherRats, Sprague-Dawleyen
dc.subject.otherSodium-Hydrogen Antiporter.metabolismen
dc.subject.otherStreptozocinen
dc.subject.otherSulfones.pharmacologyen
dc.titleDiabetes-induced vascular hypertrophy is accompanied by activation of Na(+)-H(+) exchange and prevented by Na(+)-H(+) exchange inhibition.en
dc.typeJournal Articleen
dc.identifier.journaltitleCirculation researchen
dc.identifier.affiliationDepartment of Medicine, University of Melbourne, Austin and Repatriation Medical Centre-Repatriation Campus, West Heidelberg, Australiaen
dc.description.pages1133-40en
dc.relation.urlhttps://pubmed.ncbi.nlm.nih.gov/11110770en
dc.type.austinJournal Articleen
item.openairecristypehttp://purl.org/coar/resource_type/c_18cf-
item.cerifentitytypePublications-
item.fulltextNo Fulltext-
item.grantfulltextnone-
item.languageiso639-1en-
item.openairetypeJournal Article-
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