Renal potassium adaptation: Na-K-ATPase activity along the nephron after chronic potassium loading.
To identify nephron sites where renal potassium adaptation takes place, Na-K-ATPase was measured with a micromethod along the nephron of potassium-loaded mice. A possible role of aldosterone in this process was evaluated in K-loaded animals treated concurrently with pharmacologic doses of spironolactone. Animals fed a potassium-enriched diet for at least 2 wk excreted about 90% of ingested potassium in the urine, and fractional potassium clearance averaged 87 +/- 8%, compared with 13 +/- 2% in controls. Na-K-ATPase activity per millimeter tubule length increased by 225% in the cortical collecting tubule and by 177% in the medullary collecting tubule, but was not substantially affected in other nephron segments. Stimulation of Na-K-ATPase was identical in the cortical collecting tubule of K-loaded mice treated with spironolactone. These results indicate that chronic potassium loading in the mouse results in an adaptive increase potassium loading in the mouse results in an adaptive increase in Na-K-ATPase in the collecting tubule and suggest that this nephron segment is the major site of potassium adaptation in this species. This effect appears to be independent of aldosterone.
D000251:Adenosine Triphosphatases / Q000378:metabolism; D000818:Animals; D004032:Diet; D005919:Glomerular Filtration Rate; D007668:Kidney / Q000502:physiology; D007685:Kidney Tubules, Collecting / Q000201:enzymology; D007686:Kidney Tubules, Distal / Q000201:enzymology; D007687:Kidney Tubules, Proximal / Q000201:enzymology; D008274:Magnesium / Q000494:pharmacology; D008297:Male; D051379:Mice; D009399:Nephrons / Q000201:enzymology*; D011188:Potassium / Q000494:pharmacology*; D000254:Sodium-Potassium-Exchanging ATPase / Q000378:metabolism*
D000251:Adenosine Triphosphatases; D000254:Sodium-Potassium-Exchanging ATPase; D008274:Magnesium; D011188:Potassium