Effect of ouabain and furosemide on erythrocyte sodium and phosphate transport.
The effects of ouabain and furosemide on the unidirectional efflux of sodium and phosphate ions were studied in freshly drawn human red blood cells (RBCs). In the presence of physiologic concentrations of sodium and potassium the rate of sodium efflux was reduced by 74% due to ouabain sensitivity. Furosemide (1.0 mmol/l) reduced ouabain-insensitive sodium transport rate by a further 50%. Thus, 13% of total sodium efflux was inhibited by furosemide when ouabain was present. In the absence of ouabain, however, furosemide inhibited 31% of total sodium transport, indicating that it also affected ouabain-sensitive sodium efflux. Phosphate transfer of RBCs was almost 1.0 mmol/l RBCs per hour. Erythrocyte concentration of orthophosphate, however, was only 0.59 mmol/l RBCs. Organic phosphate esters must therefore have been cleaved to maintain constant phosphate elimination. The hydrolysis of adenosine triphosphate (ATP) by Na-K-ATPase might be involved because the phosphate transfer of almost 0.12 mmol/l RBCs per hour was ouabain sensitive. Furosemide reduced phosphate efflux by 50% due to reduction in passive permeability of the RBC membrane. Additional inhibition of any phosphate ester hydrolyzing enzymatic activity cannot, however, by excluded.
D000328:Adult; D001693:Biological Transport, Active / Q000187:drug effects; D002463:Cell Membrane Permeability; D004912:Erythrocytes / Q000187:drug effects* / Q000378:metabolism; D005665:Furosemide / Q000494:pharmacology*; D006801:Humans; D007473:Ion Channels / Q000187:drug effects*; D008297:Male; D010042:Ouabain / Q000494:pharmacology*; D010710:Phosphates / Q000378:metabolism*; D011188:Potassium / Q000378:metabolism; D012964:Sodium / Q000378:metabolism*; D000254:Sodium-Potassium-Exchanging ATPase / Q000378:metabolism
D007473:Ion Channels; D010710:Phosphates; D010042:Ouabain; D005665:Furosemide; D012964:Sodium; D000254:Sodium-Potassium-Exchanging ATPase; D011188:Potassium