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dc.contributor.authorHulthén, U Len
dc.contributor.authorCao, Zeminen
dc.contributor.authorRumble, J Ren
dc.contributor.authorCooper, Mark Een
dc.contributor.authorJohnston, Colin Ien
dc.identifier.citationAmerican Journal of Hypertension; 9(9): 895-901en
dc.description.abstractThe aim of this study was to compare the effects of angiotensin converting enzyme (ACE) inhibition, angiotensin II (AII) AT1-receptor blockade, and dihydropyridine calcium antagonism on hypertrophy and on vascular albumin permeability in kidney, heart, and mesenteric artery in a model combining genetic hypertension and diabetes mellitus. Diabetes mellitus was induced by streptozotocin in 8-week-old spontaneously hypertensive rats. The animals were randomized to receive no treatment, the angiotensin converting enzyme inhibitor ramipril, the AII AT1-receptor blocker valsartan, or the dihydropyridine calcium antagonist lacidipine for 3 weeks. Vascular albumin permeability was measured as the tissue content of intravenously injected Evans blue dye (EB) in kidney, heart, and mesenteric artery and the tissue/plasma EB ratio was calculated. Systolic blood pressure was reduced by all three antihypertensive regimens. Glycemic control was similar in all diabetic groups. Kidney hypertrophy was not affected by any of the antihypertensive drugs. Hypertrophy of the mesenteric artery was enhanced by lacidipine but was not affected by ramipril or valsartan. Relative heart weight was also increased by lacidipine. Vascular albumin permeability, expressed as EB content in micrograms/gram dry weight or as tissue/plasma EB ratio, was higher in the kidneys of lacidipine-treated rats than in any other group of diabetic rats. There was a positive correlation between kidney weight/body weight and kidney/plasma EB ratio in the diabetic rats. These findings indicate that the dihydropyridine calcium antagonist lacidipine is associated with an unfavorable effect on vascular hypertrophy and on vascular albumin permeability in the kidneys in rats with hypertension and diabetes mellitus. Furthermore, there seems to be a coupling in the diabetic kidney between hypertrophy and increased vascular albumin permeability.en
dc.subject.otherAnalysis of Varianceen
dc.subject.otherAngiotensin Receptor Antagonistsen
dc.subject.otherAngiotensin-Converting Enzyme Inhibitors.pharmacologyen
dc.subject.otherAntihypertensive Agents.pharmacologyen
dc.subject.otherBlood Glucose.analysisen
dc.subject.otherBlood Pressure.drug effectsen
dc.subject.otherCapillary Permeability.drug effectsen
dc.subject.otherColoring Agents.analysisen
dc.subject.otherCoronary Vessels.drug effects.metabolismen
dc.subject.otherDiabetes Mellitus, Experimental.physiopathologyen
dc.subject.otherEvans Blue.analysisen
dc.subject.otherKidney.blood supply.pathologyen
dc.subject.otherMesenteric Arteries.metabolismen
dc.subject.otherRats, Inbred SHRen
dc.subject.otherReceptor, Angiotensin, Type 1en
dc.subject.otherReceptor, Angiotensin, Type 2en
dc.subject.otherSerum Albumin.metabolismen
dc.subject.otherValine.analogs & derivatives.pharmacologyen
dc.titleVascular hypertrophy and albumin permeability in a rat model combining hypertension and diabetes mellitus. Effects of calcium antagonism, angiotensin converting enzyme inhibition, and angiotensin II-AT1-receptor blockade.en
dc.typeJournal Articleen
dc.identifier.journaltitleAmerican Journal of Hypertensionen
dc.identifier.affiliationDepartment of Medicine, University of Melbourne, Austin and Repatriation Medical Centre, Heidelberg, Victoria, Australiaen
dc.type.austinJournal Articleen
item.fulltextNo Fulltext-
item.openairetypeJournal Article-
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