Korean Journal of Nephrology 1993;12(3):295-303.
급성 허혈성 신부전에서 Na -K ATPase의 변화
정태시 , 김창수 , 진동규 , 석준 , 차대룡 , 권영주 , 조원용 , 김형규
Abstract
Background
Acute renal failure is a clinical syn- drome characterized by a rapid deterioration in renal function, resulting in the failure of the kidney to excrete nitrogenous waste products. Ischemia is the most com- mon cause of ARF. Renal ischemia occurs in response to a wide range of insults such as impaiiment of the sys- temic circulation, stenosis of the renal artery, conges- tive heart failure, liver cirrhosis, and septic shock. In renal tubular epithelia, Na-K ATPase is located exclu- sively on basolateral membranes and transports sodium ions out of, arid potassium ions into the cytosol. This ATPase plays an important role in the reabsorption of sugars, amino acids and numeraus other solutes in the kidney. Ischemia results in duration dependent loss of epithelial cell polarity. Loss of surface membrane polar- ity is preceded by disruption of cellular tight junction. During recovery from ischemic injury, reaal tubular cells undergo remodelling of the surface membrane, allowing for the return of normal cellular fenction. So authors purposed to investigate the changes of Na-K ATPase during acute ischemic renal failure Methods: The experimental animals, rats, were divided into three groups. Group I(n=5) was control without any procedure, Group II(n = 6) was shame opera- tion group without renal artery clamping, Group III (n = 12) was ischemic ARF model by renal artery clamping for 40 minutes. In ischemic renal failure rrwdel, half of the rats underwent 1 hour of reperfusion and another half underwent 24 hours of reperfusion and then kidney was fixed with 2% paraformaldehyde and 0.25% glutar- aldehyde as fixatives using whole body perfusion fixa- tion method via aortic cannulation. Measurement of Na-K ATPase activity was performed esing a cyto- chemical method, based on measurement of inorganic phosphate generated during ATP hydrolysis by ATPase during the incubation period in the presenee of a lead ammonium citrate acetate complex. Results: The mean serum creatinine level in each group revealed as follows; 0.44±0.22 mg/dl in control group, 0.46 0.10 mg/dl in shame operation group, 0.80± 0.21 mg/dl in the ischemic group after 1 hwr of reper- fusion, 2.90±1.05 mg/dl in the ischemic group after 24 hours of reperfusion. The reaction products of Na-K ATPase were irregular in shape, and distributed mainly in the basolateral membranes of thick ascending limb of loop of Henle, distal convoluted tubules and proximal convoluted tubules in the control group. After 40 min- utes of ischemia, almost all structures had markedly decreased the reaction products, and focally Na-K ATPases were translocatted in the luminal nembranes. There were no significant differences in the reactivity and the distribution of Na-K ATPase according to the reperfusion time in the ischemic groups. Conclusion: These results suggest that Na-K ATPases were translocatted to luminal surface from basolateral surface after renal ischemia. The changes in the loca- tion of Na-K ATPase during acute ischemic renal fail- ure might be related with disruption of intercellular tight junction. These changes were not affected by reperfusion time after renal ischemia.
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