Abstract
Abstract
The effect of chronic salt loading in rats fed regular chow diet on renal Na-K-ATPase was studied. The high salt intake was associated with increased filtered load of sodium (control: 126 ± 3.9 μeq/min, salt loaded: 146 ± 2.5, μeq/min, P < 0.001), increased net reabsorption of sodium (control: 125.3 ± 3.9 μeq/min, salt load: 134.8 ± 2.4 μeq/min, P < 0.05), increased urinary excretion of potassium (control: 2.4 ± 0.09 μeq/min; salt loaded: 3.0 ± 0.1 μeq/min, P < 0.001) and increase in single kidney weight (control: 0.798 ± 0.010 g, salt loaded: 0.937 ± 0.015 g, P < 0.001). The above mentioned changes were associated with significant increase in renal microsomal and whole homogenate medullary Na-K-ATPase activity in the salt loaded group (microsomes: control 74.1 ± 4.9 μmole P i/mg prot/hr, salt loaded 112.7 ± 6.0 μmole P i/mg prot/hr, P < 0.001; whole homogenate: control 22.7 ± 1.0 μmole P i/mg prot/hr, salt load 29.4 ± 1.6 μmole P i/mg prot/hr, P < 0.005), while cortical and papillary Na-K-ATPase activity remained unchanged. Taken together, these results show that increased filtered and reabsorbed load of sodium, which follows high salt intake, is associated with an increased renal Na-K-ATPase activity. The preferential rise in medullary enzymatic activity may be interpreted as suggesting that these changes may stem from increased delivery and reabsorption of sodium in the ascending limb of Henle's loop.
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