ABSTRACT
Background. The pathophysiology of renal impairments occurring in obstructive jaundice has been extensively studied, but underlying mechanism of these derangements remains unclear. The aim of the present study was to investigate the time-related morphological and functional changes occurring in the kidneys of rats undergoing obstructive jaundice. Methods. Histological examination, renal function assessment and determination of (Na + K)-ATPase activity were performed in the kidneys of rats 7, 14, and 21 days following bile duct ligation (BDL) or sham operation (sham). Results. Glomerular filtration rate was unaffected by BDL throughout the period of the study. Tubular effects occurred at days 7 ant 14, being more marked at day 7, and consisted of an increase of about twice in the fractional excretion of sodium and chloride, paralleled by a decreased proximal and distal tubular reabsorption of sodium of about 50 and 40 percent, respectively. Natriuresis was consistent with augmentation of osmolar clearance but it was not associated with changes in the acivity of renal (Na+ + K+)-ATPase. The ability to dilute urine was imparied at days 14 and 21 after BDL. Additionally, these effects were accompanied by decreased tubulointerstitial fibrosis and vasodilation of inner medullary capillaries. At day 21, the parameters of tubular function in BDL and sham groups were not significantly different. Conclusions. These data support the view that rasied natriuresis taking place in the initial 2 weeks following BDL is due mainly to tubular effects. The contribution of hemodynamic, paracrine and humoral mediators is discussed
Subject(s)
Animals , Male , Rats , Bilirubin/metabolism , Cholestasis/physiopathology , Kidney/physiopathology , Cholestasis/metabolism , Cholestasis/pathology , Rats, Wistar , Sodium-Potassium-Exchanging ATPase/metabolismABSTRACT
Background. The effect of bromoethylamine (BEA) administration on lipid peroxidation and on the activieties of antioxidant enzymes was studied. Methods. Adult rats received BEA at 1.2 mmol/kg, a dose that produces renal papillary necrosis. Lipid peroxidation assessed by maximal rate in MDA formation, the activities of catalase, superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px), and the levels of non-protein sulfhydryls (NPSH) were measured in renal cortex and papilla of control and BEA-treated animals. Results. After BEA treatment, an increment in lipid peroxidation in papilla and cortex was found after 1.5 and 24 hours of treatment. Catalase activity decreased in both regions, but earlier cortex. Conclusion. These data suggest some role of oxidative stress in the mechanism of BEAinduced papillary necrosis
Subject(s)
Animals , Female , Rats , Antioxidants/metabolism , Catalase/metabolism , Ethylamines/toxicity , Glutathione Peroxidase/metabolism , Kidney Papillary Necrosis/chemically induced , Superoxide Dismutase/metabolism , Kidney Cortex/enzymology , Kidney Medulla/enzymology , Kidney Papillary Necrosis/enzymology , Malondialdehyde/analysis , Organ Specificity , Oxidative Stress , Rats, Sprague-Dawley , Sulfhydryl Compounds/analysisABSTRACT
A method was devised to determine the nature of the mechanism of the increase in renal (NA++K+)-ATPase in rats fed dilute ethanol for ten weeks. Antiserum to (NA++K+)-ATPase obtained from rabbits was added to microssomal fractions of Kidney and the activities of (NA++K+)-ATPase and Mg2+ ATPase were determined. The addition of antiserum resulted in a same pattern of dose-related inhibition of (NA++K+)-ATPase activity in control and ethanol-fed rats, whereas mg2+-ATPase was not affected by the antiserum. These results suggest that the mechanism of ethanol-induced enhancement of renal (NA++K+)-ATPase activity could be explained through an increase in the number of catalytic units.