6533b7d2fe1ef96bd125ebec

RESEARCH PRODUCT

Red blood cell sodium and potassium after hydrochlorothiazide.

U Walter

subject

PharmacologyIntracellular sodiumMaleErythrocytesTime FactorsPotassiumSodiumSodiumchemistry.chemical_elementPharmacologyRed blood cellHydrochlorothiazidemedicine.anatomical_structureHydrochlorothiazidechemistrySerum potassiummedicinePotassiumHumansPharmacology (medical)EffluxInhibitory effectmedicine.drug

description

In six of seven healthy males 6 days of hydrochlorothiazide (HCT), 50 mg twice daily, without potassium supplements resulted in a rise in red blood cell (RBC) sodium concentration. Serum potassium concentration fell in all subjects. Four days after discontinuing HCT, intracellular sodium and extracellular potassium concentrations had normalized. Throughout the evaluation period the course of mean relative intracellular sodium was almost a mirror image of mean relative extracellular potassium. Thus, either the decline of serum potassium or of HCT (because of its inhibitory effect on Na-K-ATPase activity) might have diminished Na-K-ATPase–dependent active RBC sodium efflux with a resultant rise in erythrocyte sodium concentration. RBC potassium and serum sodium concentrations were not affected by short-term exposure to HCT. Clinical Pharmacology and Therapeutics (1981) 30, 373–377; doi:10.1038/clpt.1981.175

yearjournalcountryeditionlanguage
1981-09-01Clinical pharmacology and therapeutics
10.1038/clpt.1981.175https://pubmed.ncbi.nlm.nih.gov/7273602