Multiple pumps for sodium reabsorption by the perfused kidney.
Several distinct transport mechanisms responsible for sodium reabsorption by the rat kidney can be identified by studying the function of isolated perfused kidneys. Approximately one-half of the fractional sodium reabsorption by the isolated perfused rat kidney appears to depend on Na-K-adenosine triphosphatase (AT-Pase) and is inhibited by ouabain. About 10 to 20% is associated with the reabsorption of bicarbonate and is blocked by acetazolamide. This fraction of transported sodium is unaffected by ouabain and therefore does not involve Na-K-ATPase. Neither furosemide nor ethacrynic acid produce further inhibition of sodium reabsorption in a kidney already exposed to ouabain and acetazolamide. Most of the residual transport of sodium is inhibited by cooling the perfused kidney, suggesting that it is powered by metabolic rather than physical sources of energy.
D000086:Acetazolamide / Q000494:pharmacology; D000251:Adenosine Triphosphatases / Q000378:metabolism; D000818:Animals; D001639:Bicarbonates / Q000378:metabolism; D005665:Furosemide / Q000494:pharmacology; D005919:Glomerular Filtration Rate / Q000187:drug effects; D007668:Kidney / Q000378:metabolism / Q000502:physiology*; D008297:Male; D010042:Ouabain / Q000494:pharmacology; D010477:Perfusion; D011188:Potassium / Q000378:metabolism; D051381:Rats; D012964:Sodium / Q000378:metabolism*; D014867:Water / Q000378:metabolism
D001639:Bicarbonates; D014867:Water; D010042:Ouabain; D005665:Furosemide; D012964:Sodium; D000251:Adenosine Triphosphatases; D000086:Acetazolamide; D011188:Potassium