Expression Of Sodium Transporters And Aquaporins In Kidney Of Rat With Acute Renal Failure

Body fluid equilibrium and homeostasis depend on reabsorption and secretion of sodium and water in kidney.Reabsorption of sodium and water is mainly accomplished by sodium transporter proteins and aquaporin proteins which expressed in different renal tubule segments,the level of sodium transporter and aquaporin and theirs location in renal tubule is also very important for reabsorption of sodium and water.Acute renal failure(acute renal failure,ARF)refers to the pathological process of rapid deterioration of renal function within the short term and the sharp disturbance of homeostasis resulted from various factors.And its clinical manifestations,such as change of urine volume,plasma and urine electrolyte levels and the accumulation of metabolic poisons,is directly related with the causes.Kidney disease manifests the water and electrolyte metabolic disorders, and this is mainly related with the expression and location of NKCC2,NCC, ENaC and AQPs in the epithelial cells of distal nephron,the abnormal expression or location of all of these protein will result in the abnormal absorption or secretion of sodium or water.In this study,following the establishment of acute renal failure animal model,in order to study the trafficking of NKCC2 and ENaC,their expression and location in the distal nephron was determined.Due to the reabsorption of sodium coupling with water metabolism,the expression of AQP2 and AQP4 was also study in this subject.The results of this experiment are helpful to explaining the mechanism of water and salt metabolism in diseased state and guiding the therapy of kidney diseases.After the establishment of the experimental rat model of acute renal failure,urine volume,serum and urine sodium,potassium and others factors was analyzed,the mRNA and protein level of sodium transporter NKCC2, γENaC and Water channel protein AQP2,AQP4 was also determined with the methods of RT-PCR,immunohistochemistry and western blotting.Results:The significant pathological alteration was shown in the kidney tissues of rat with ARF.The urine volume decreased at first,but increased gradually in ARF rat.When compared with the control rats,the expression of NKCC2,AQP2 and AQP4 mRNA increased significantly in kidney tissues of the experimental group(p＜0.05).And the increasedγENaC expression of ARF rats was further proved with the immunohistochemistry and Western blotting methods,the ratio of membrane of NKCC2 andγENaC in tubular epithelial cells increased more obvious when comparing the ratio of plasma and membrane protein.Conclusion:The pathological finding and changes in urine volume supports that glycerol can successfully induce acute renal failure of rats,rats with ARF mainly manifests the renal concentration deficiency.During ARF period,the mRNA of sodium transporter and water channel increased,and both membrane and cytoplasm NKCC2,γENaC expression increased also,and the increased membrane protein is the key step for sodium reabsorption.The compensatory enhanced function of part of nephron with normal structure, such as the enhanced activity,membrane location or the increased level of sodium transporter and the water channel protein,involved in the metabolism of sodium and water in the diseased kidney.