Atrial natriuretic factor ameliorates chronic metabolic alkalosis by increasing glomerular filtration.
The kidney maintains the elevated plasma concentration of bicarbonate that occurs in chronic metabolic alkalosis. A reduction in the glomerular filtration rate (GFR) can maintain the filtered bicarbonate load at a normal level so that a normal rate of bicarbonate reabsorption suffices to prevent urinary excretion of this anion. It is also possible that bicarbonate reabsorption might increase so as to maintain the alkalosis if GFR were not reduced. To examine this latter possibility, atrial natriuretic factor was used in alkalotic rats to restore a more normal GFR and to increase the amount of bicarbonate filtered by the glomerulus. Proximal bicarbonate reabsorption remained relatively static. Higher than normal amounts of bicarbonate were then delivered out of the proximal tubule, bicarbonate appeared in the urine, and the plasma concentration of bicarbonate fell. A reduction in GFR is thus necessary for the maintenance of chronic metabolic alkalosis. Normalizing GFR induces bicarbonaturia and initiates repair of the alkalosis.
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D000471:Alkalosis / Q000188:drug therapy* / Q000503:physiopathology; D000818:Animals; D009320:Atrial Natriuretic Factor; D001639:Bicarbonates / Q000652:urine; D002712:Chlorides / Q000652:urine; D005110:Extracellular Space / Q000187:drug effects; D005919:Glomerular Filtration Rate / Q000187:drug effects*; D007668:Kidney / Q000187:drug effects / Q000503:physiopathology; D009124:Muscle Proteins / Q000494:pharmacology* / Q000627:therapeutic use; D009399:Nephrons / Q000187:drug effects / Q000502:physiology; D051381:Rats
D001639:Bicarbonates; D002712:Chlorides; D009124:Muscle Proteins; D009320:Atrial Natriuretic Factor