TL;DRAbstract
A majority of patients with chronic kidney disease (CKD) die of cardiovascular (CV) disease before reaching end-stage renal disease. The causes of CV death in CKD are characterized by an excess of sudden cardiac deaths compared to the general population. Arterial defects that are typical in these patients are aortic stiffness and media calcifications. Maladaptive changes in vascular smooth muscle cells (VSMCs) take place in response to mineral metabolism disorders that develop with declining kidney function. \nThe aims of the present studies were: 1) to investigate the effects of chronic renal failure (CRF) on resistance arteries and aorta in rats with adenine-induced CRF (A-CRF); 2) to determine by which mechanisms A-CRF rats develop hypertension and to investigate whether reduced aortic relaxation rate is associated with increased aortic stiffness; 3) to investigate the presence of reduced relaxation rate in other conduit arteries and to elucidate underlying mechanisms of this vascul
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A majority of patients with chronic kidney disease (CKD) die of cardiovascular (CV) disease before reaching end-stage renal disease. The causes of CV death in CKD are characterized by an excess of sudden cardiac deaths compared to the general population. Arterial defects that are typical in these patients are aortic stiffness and media calcifications. Maladaptive changes in vascular smooth muscle cells (VSMCs) take place in response to mineral metabolism disorders that develop with declining kidney function. \nThe aims of the present studies were: 1) to investigate the effects of chronic renal failure (CRF) on resistance arteries and aorta in rats with adenine-induced CRF (A-CRF); 2) to determine by which mechanisms A-CRF rats develop hypertension and to investigate whether reduced aortic relaxation rate is associated with increased aortic stiffness; 3) to investigate the presence of reduced relaxation rate in other conduit arteries and to elucidate underlying mechanisms of this vascul
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