Defect in urinary acidification induced in vitro by amphotericin B.
An experimental defect in urinary acidification was induced in the isolated turtle bladder by amphotericin B and the nature of the defect was examined. Net hydrogen ion secretion was little affected by amphotericin when passive electrochemical forces across the epithelium were held at a minimum in the short-circuited state under isohydric conditions. Hydrogen ion secretion against a gradient, however, was markedly reduced by amphotericin and abolished at gradients of more than 2 pH units.The results suggest that impaired acidification is caused by increased passive permeability of the luminal membrane and increased back diffusion of hydrogen ion rather than by failure of active transport. This interpretation is supported by evidence that amphotericin causes a large increase in the permeability to potassium and smaller increases in the sodium and chloride permeabilities. This mechanism of impaired acidification in vitro may have bearing on the renal tubular defect observed in patients treated with amphotericin B.
D000141:Acidosis, Renal Tubular / Q000139:chemically induced; D000143:Acids / Q000378:metabolism*; D000666:Amphotericin B / Q000009:adverse effects* / Q000494:pharmacology; D000818:Animals; D002712:Chlorides / Q000378:metabolism; D004594:Electrophysiology; D004848:Epithelium / Q000187:drug effects / Q000502:physiology; D006859:Hydrogen / Q000378:metabolism; D006863:Hydrogen-Ion Concentration; D066298:In Vitro Techniques; D007684:Kidney Tubules / Q000187:drug effects* / Q000502:physiology; D010539:Permeability; D012964:Sodium / Q000378:metabolism; D014426:Turtles; D001743:Urinary Bladder / Q000187:drug effects / Q000502:physiology
D000143:Acids; D002712:Chlorides; D000666:Amphotericin B; D006859:Hydrogen; D012964:Sodium