Activation of epithelial Na channels during short-term Na deprivation

The role of epithelial Na channels in the response of the kidney to short-t erm Na deprivation was studied in rats. Animals were fed either a control-N a (3.9 g/kg) or a low-Na (3.8 mg/kg) diet for 15 h. Urinary excretion of Na (mmol/min), measured in conscious animals in metabolic cages, was 0.45 +/- 0.07 in controls and 0.04 +/- 0.01 in Na-deprived animals. Glomerular filt ration rate, measured as the clearance of creatinine, was unaffected by the change in diet, suggesting that the reduced Na excretion was the result of increased Na reabsorption. K excretion (mmol/min), increased after the 15- h period of Na deprivation from 0.70 +/- 0.10 to 1.86 +/- 0.19. Thus the de crease in urine Na was compensated for, in terms of electrical charge balan ce, by an increase in urine K. Plasma aldosterone increased from 0.50 +/- 0 .08 to 1.22 +/- 0.22 nM. Principal cells from cortical collecting tubules i solated from the animals were studied by using the patch-clamp technique. W hole cell amiloride-sensitive currents were negligible in the control group (5 +/- 4 pA/cell) but substantial in the Na-deprived group (140 +/- 28 pA/ cell). The abundance of the epithelial Na channel subunits, alpha, beta, an d gamma in the kidney was estimated by using immunoblots. There was no chan ge in the overall abundance of any of the subunits after the 15-h Na depriv ation. However, the apparent molecular mass of a fraction of the gamma -sub units decreased as was previously reported for long-term Na deprivation. Ca lculations of the rate of Na transport mediated by the Na channels indicate d that activation of the channels during short-term Na deprivation could ac count in large part for the increased Na reabsorption under these condition s.