High-NaCl diet impairs dynamic renal blood flow autoregulation in rats with adenine-induced chronic renal failure

摘要

The overall objective of the present study was to examine kidney function and dynamic RBFA in rats with adenine-induced chronic renal failure (ACRF) and to determine the impact of a high dietary NaCl intake. Following dietary intake, adenine is metabolized to 2,8-dihydroxyadenine, which is freely filtered by the glomeruli and crystallizes in tubular fluid leading to tubular obstruction and chronic tubulointerstitial injury (39). Rats with ACRF develop severe renal insufficiency and metabolic abnormalities resembling those typically observed in patients with uremia (14, 23, 24, 27-31), making it an attractive model for investigating pathophysiological mechanisms in chronic renal failure (CRF). The model of ACRF has mainly been used to examine the effects of severe renal failure on mineral and bone metabolism and extraosseous calcifications (14, 23, 24, 27-29). Only a limited number of studies have investigated kidney function and renal hemodynamics in detail in this model (13, 19). The model of ACRF may show a higher resemblance to the clinical situation in CRF patients compared with the remnant kidney model, as rats typically develop more pronounced reductions in GFR (30, 31). In addition, kidney failure in ACRF rats is caused by homogenous parenchymal injury and not by removal of tissue mass by surgery or renal infarction.