Regulations of Bicarbonate Ions in Hypokalemic Rat Kidney / 대한해부학회지

ABSTRACT

A number of acid-base or electrolyte disorders are associated with decreased or increased HCO3- reabsorption in the renal tubules. There has been a general agreement that potassium depletion induces and maintains metabolic alkalosis in rats. However, many researchers have approached such issue only from functional studies to investigate Na+/H+ exchanger (NHE-3) and Na+/HCO(3-) cotransporter (NBC) activity which closely relates to potassium depletion. In addition the results obtained vary according to their researchers. Thus the present study was employed Western blot analysis and immunohistochemistry together, to examine the alterations of expression and distribution of NHE-3 and NBC-1 with reference to HCO3- reabsorption in the kidneys of rats fed potassium free diets according to the periods. Western blot analysis demonstrated that NHE-3 protein, ~83 kDa at molecular mass, was abundantly expressed in normal group. All potassium-depleted groups showed significantly increased NHE-3 protein compared to normal group. NBC-1 protein, ~110 kDa at molecular mass, was moderately expressed in normal group. All potassium-depleted groups had much higher amounts of the protein than normal group. There was a highly increased amount of NBC-1 protein especially in K-depleted 1 week group. Immunohistochemistry showed positive immunoreactivity of NHE-3 in the apical membranes and brush borders of proximal renal tubule cells. Its reactivity was most prominent in the S3.S1 and S2 had moderate immunoreactivity. Potassium-depleted groups had an identical pattern of cellular labeling of NHE-3 protein compared with that of normal group. However the signal intensity of NHE-3 protein in potassium-depleted groups was much higher than that of normal group. Immunoreactivity of NBC-1 was observed exclusively in the basolateral plasma membranes of proximal tubule cells. There was a strong reactivity in the S1 and S2, whereas S3 did not show any reactivity. Potassium-deprived rats exhibited an identical pattern of cellular labeling of NBC-1 protein compared with that of normal rats. However, the signal intensity of NBC-1 protein was markedly increased in potassium-deprived rats. These results suggest that increased NHE-3 and NBC-1 expression resulted from potassium depletion in the renal proximal tubules, enhances HCO3-reabsorption and consequently maintains metabolic alkalosis.