REGULATION OF BODY WATER AND ELECTROLYTES CONCENTRATIONS BY RENAL NA/K/2CL TRANSPORTER (NKCC2)

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It is known that abundance of the membrane transporter gene expression in kidney tubules changes during the period of either growing or aging. Its level is provably regulated by changes in the chemical or hormonal conditions of internal environment. Physiological and pathological changes in body fluid electrolytes, which are related with food intake, internal metabolism, and various diseases, may directly affect expression of the ion transporter mRNA.In order to investigate the factors which may regulate the gene expression, we have prepared two model animals : one is the potassium-loaded newborn rat and the other one is the rat with cardiac infarction. First, development of the renal potassium excretion capacity was studied in the newborn rats of 7-14 days which were acutely infused with the exogenous potassium. The onset of the extra potassium excretion was determined as 1.7 day. Time-course of the ROMK1 expression was in parallel increased with that of the extra potassium excretion. Time-courses of the ROMK2 and Kir7.1 expression were different. According to these results, a possible rate limiting step for potassium secretion is hypothesized as ROMK1 channel at the apical membrane of collecting ducts. Second, time-dependent changes in the expression of NHE1 mRNA and protein were investigated by using either RNase protection assay or Western blotting, respectively, in the rat with cardiac infarction. It seems to be strange that NHE1 protein decreased significantly at 5 h after the infarction, whereas NHE1 mRNA varied little in the same period. Decrease in sodium influx through a N+/H+ antiporter may protect the cardiac cell by decreasing ATP consumption of Na+/K+ ATPase. Regulation of the Na/K/2Cl transporter (NKCC2) mRNA expression by the secondary changes in electrolytes after cardiac infarction remains unsolved.