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dc.contributor.authorSeyed Shobeiri, Naviden
dc.date2009-12-16 15:10:49.384
dc.date.accessioned2009-12-17T15:18:33Z
dc.date.available2009-12-17T15:18:33Z
dc.date.issued2009-12-17T15:18:33Z
dc.identifier.urihttp://hdl.handle.net/1974/5359
dc.descriptionThesis (Master, Pharmacology & Toxicology) -- Queen's University, 2009-12-16 15:10:49.384en
dc.description.abstractChronic kidney disease (CKD) is a worldwide health problem with rising incidence and high cardiovascular mortality. CKD compromises cardiovascular function, in part, characterized by vascular calcification (VC), elevated pulse wave velocity (PWV) and pulse pressure (PP). Through manipulation of dietary adenine, we produced a model characterized by graded severity of CKD, VC and hyperphosphatemia. To our knowledge, we are the first to explore the relationship between aortic calcium content and changes in circulatory function in rodents with CKD. Fourteen-week old Sprague-Dawley rats received a diet containing an adenine concentration (0.25-0.75%) plus high-normal dietary phosphate (1%), for up to 10 weeks. Circulatory changes were determined by arterial radiotelemetry (n=6) and by assessment of aortic pulse wave velocity (PWV, n=32). VC was assessed using the calcium-O-cresophthalein-complexone assay. At sacrifice, kidney function (creatinine (µmol/L)) was worst in the group with VC (251.3±60.2 µmol/L), compared to non-calcifying CKD (200.3±68.8 µmol/L) or control (50.0±16.2 µmol/L). PWV (cm/s) adjusted for blood pressure (BP) was markedly elevated in animals with VC (3.23±0.33 log(cm/s)) versus non-calcifying CKD (2.85± 0.12 log(cm/s)) or control (2.96±0.08 log(cm/s)). Arterial pressure radiotelemetry revealed that there was an increase in pulse pressure (38±4.7 mmHg to 58 ±15.2 mmHg) during the development of VC. Systolic pressure remained relatively stable throughout (129±8.7 mmHg), diastolic pressure fell during weeks 9 and 10 of the study (91±6.0 mmHg down to 74±9.1 mmHg), a fall that almost fully accounted for the changes in pulse pressure. The calcifying CKD animals also exhibited left ventricular hypertrophy (LVH) compared to CKD or control animals (2.32±0.3 vs 2.03±0.2, 1.80±0.1 g/kg respectively). Manipulating dietary adenine produces a graded severity of CKD with calcification which impact circulatory changes (PP and PWV). These altered circulatory functions are likely to be key factors in the enhanced LVH. This model appears to be a useful for the study of CKD-associated VC.en
dc.format.extent610523 bytes
dc.format.mimetypeapplication/pdf
dc.language.isoengen
dc.relation.ispartofseriesCanadian thesesen
dc.rightsThis publication is made available by the authority of the copyright owner solely for the purpose of private study and research and may not be copied or reproduced except as permitted by the copyright laws without written authority from the copyright owner.en
dc.subjectChronic Kidney Diseaseen
dc.subjectVascular Calcificationen
dc.subjectAdenine Dieten
dc.subjectRatsen
dc.titleCharacterization of Vascular Calcification in a Rodent Model of Chronic Kidney Diseaseen
dc.typethesisen
dc.description.degreeM.Sc.en
dc.contributor.supervisorAdams, Michael A.en
dc.contributor.supervisorHolden, Rachel M.en
dc.contributor.departmentPharmacology and Toxicologyen
dc.degree.grantorQueen's University at Kingstonen


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