Abstract
In this study erythrocyte phosphate release depended on the intracellular hydrolysis of organic phosphate esters. Total phosphate release was increased in essential hypertension, which suggests an elevated phosphate ester metabolism. Ouabain-sensitive phosphate release was decreased, and the ratio of intracellular Na+/K+ concentrations was increased, a finding consistent with a diminished Na-K-ATPase activity. Furosemide in a concentration of 1.0 mmol/L inhibited erythrocyte phosphate release by half, probably owing to nonspecific membrane effects. The combination of ouabain and furosemide reduced phosphate transfer to a higher degree than did each substance individually. Because of the nonspecific alteration of erythrocyte membrane permeability by furosemide in a concentration of 1.0 mmol/L, ouabain-insensitive, furosemide-sensitive phosphate release and ouabain-insensitive, furosemide-sensitive Na+ efflux (Na-K cotransport) must not be regarded uncritically as specific transport systems.
Publisher
Ovid Technologies (Wolters Kluwer Health)
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