title: Activation of epithelial Na channels during short-term Na deprivation.
abstract: The role of epithelial Na channels in the response of the kidney to short-term Na deprivation was studied in rats. Animals were fed either a control-Na (3.9 g/kg) or a low-Na ( 3.8 mg/kg) diet for 15 h. Urinary excretion of Na (micromol/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 filtration 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 (micromol/min), increased after the 15-h period of Na deprivation from 0.70 +/- 0.10 to 1.86 +/- 0.19. Thus the decrease in urine Na was compensated for, in terms of electrical charge balance, 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 isolated from the animals were studied by using the patch-clamp technique. Whole 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, and gamma in the kidney was estimated by using immunoblots. There was no change in the overall abundance of any of the subunits after the 15-h Na deprivation. However, the apparent molecular mass of a fraction of the gamma-subunits decreased as was previously reported for long-term Na deprivation. Calculations of the rate of Na transport mediated by the Na channels indicated that activation of the channels during short-term Na deprivation could account in large part for the increased Na reabsorption under these conditions.
authors.affiliation: Department of Physiology and Biophysics, Weill Medical College of Cornell University, New York, New York 10021, USA.
authors.forename: G
authors.initials: G
authors.lastname: Frindt
authors.forename: S
authors.initials: S
authors.lastname: Masilamani
authors.forename: M A
authors.initials: MA
authors.lastname: Knepper
authors.forename: L G
authors.initials: LG
authors.lastname: Palmer
mesh_terms: D000450:Aldosterone / Q000097:blood; D000584:Amiloride / Q000494:pharmacology; D000818:Animals; D003404:Creatinine / Q000378:metabolism; D004039:Diet, Sodium-Restricted; D005260:Female; D005919:Glomerular Filtration Rate / Q000502:physiology*; D007672:Kidney Cortex / Q000502:physiology*; D007685:Kidney Tubules, Collecting / Q000502:physiology*; D008297:Male; D008564:Membrane Potentials / Q000187:drug effects / Q000502:physiology; D011188:Potassium / Q000097:blood; D021122:Protein Subunits; D051381:Rats; D017207:Rats, Sprague-Dawley; D012964:Sodium / Q000097:blood / Q000378:metabolism* / Q000652:urine; D015222:Sodium Channels / Q000187:drug effects / Q000502:physiology*; D013997:Time Factors; D019459:Urothelium / Q000502:physiology
chemical_list: D021122:Protein Subunits; D015222:Sodium Channels; D000450:Aldosterone; D000584:Amiloride; D012964:Sodium; D003404:Creatinine; D011188:Potassium