Thesis (Ph. D.)--University of Washington, 2003. / Vita. Includes bibliographical references (leaves 97-114).

Chronic 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. / Thesis (Master, Pharmacology & Toxicology) -- Queen's University, 2009-12-16 15:10:49.384

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Thesis (Ph.D.)--University of Adelaide, Dept. of Physiology, 2003? / Includes bibliographical references (leaves 226-273.). Also available in an electronic version.

Thesis (Ph.D.)--University of Adelaide, Dept. of Physiology, 2002. / Includes bibliographical references. Also available in a print form.

Thesis (M.Sc.). / Written for the Dept. of Human Genetics. Title from title page of PDF (viewed 2008/07/30). Includes bibliographical references.

Thesis (Ph.D.) - University of St Andrews, November 2007.

Thesis (M.S.)--University of Michigan, 1960.

Thesis (Ph. D.)--University of Washington, 2000. / Vita. Includes bibliographical references (leaves 174).

Thesis (Ph. D.)--University of Washington, 2006. / Vita. Includes bibliographical references (leaves 112-139).