In renal failure, parathyroid hormone (PTH) is not only involved in the genesis of disturbed calcium/phosphate metabolism and ostitis fibrosa; it is also a permissive factor in the genesis of hypertension, cardiovascular damage, and dyslipidemia. The allosteric activator of the calcium sensing receptor NPSR-568 (R-568) has been shown to reduce the serum intact PTH (iPTH) concentration in uremic rats. It was the purpose of this study in subtotally nephrectomized (SNX) rats to compare pharmacologic abrogation of secondary hyperparathyroidism by R-568 with parathyroidectomy (PTX).
View Article and Find Full Text PDFKidney Blood Press Res
September 2003
Background: Early glomerular hypertrophy and late glomerulosclerosis have been observed in rats fed high fructose diet (HFD), comparable with those of diabetic rats. Several studies suggest a role for nitric oxide (NO) in the pathogenesis of renal damage in diabetes. This study investigated the possible role of NO in the pathogenesis of HFD-induced glomerular changes.
View Article and Find Full Text PDFBackground: The effect of the specific endothelin (A) (ET(A))-receptor antagonist LU 302146 (LU) was assessed in a normotensive model of chronic transplant vasculopathy, i.e. orthotopic allotransplantation of the infrarenal abdominal aorta from spontaneously hypertensive-to-Wistar-Kyoto (SHR-to-WKY) rats.
View Article and Find Full Text PDFBackground: Cigarette smoking increases the risk of progression of diabetic and non-diabetic renal diseases. The mechanisms underlying the adverse effects of smoking are largely unknown. We examined the subtotally nephrectomized rat (i) to investigate whether components of cigarette smoke dissolved in acetone (cigarette smoke condensate) aggravate structural renal damage and (ii) to establish whether this provides an animal model that can be used to investigate potential pathomechanisms of cigarette smoke-induced renal damage.
View Article and Find Full Text PDFBackground: Specific endothelin A (ET(A))-receptor blockade and ACE inhibition attenuate chronic transplant nephropathy (CTN) in the 'Fisher-to-Lewis' rat model. It is unknown (i) which of both pharmacological interventions attenuates CTN more effectively and (ii) whether combination therapy exerts additive nephroprotection.
Methods: We compared (i) the effects of specific ET(A)-receptor blockade with LU 302146 (30 mg/kg bw/day) and ACE inhibition with trandolapril (0.