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10.1016/0005-2736(90)90139-f

http://scihub22266oqcxt.onion/10.1016/0005-2736(90)90139-f
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2139797!ä!2139797

suck abstract from ncbi


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pmid2139797      Biochim+Biophys+Acta 1990 ; 1023 (3): 455-61
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  • Characterization of Na(+)-dependent Mg2+ efflux from Mg2(+)-loaded rat erythrocytes #MMPMID2139797
  • Gunther T; Vormann J; Hollriegl V
  • Biochim Biophys Acta 1990[Apr]; 1023 (3): 455-61 PMID2139797show ga
  • Na(+)-dependent Mg2+ efflux from Mg2(+)-loaded rat erythrocytes was determined from the increase of extracellular Mg2+ concentration or decrease of intracellular Mg2+ content, as measured by means of atomic absorption spectrophotometry. Mg2+ efflux was specifically combined with the uptake of Na+ at a stoichiometric ratio of 2Na+:1Mg2+, indicating electroneutral Na+/Mg2+ antiport. Na+/Mg2+ antiport depended on intracellular ATP and was inhibited by amiloride and quinidine, but was insensitive to strophanthin. Net Mg2+ efflux was only occurring at increased concentration of intracellular Mg2+ ([Mg2+]i), and stopped when the physiological Mg2+ content was reached. Intracellular Mg2+ acted cooperatively with a Hill coefficient of 2.4, which may indicate gating of Na+/Mg2+ antiport at increased [Mg2+]i. At increased intracellular Na+ concentration, Na+ competed with intracellular Mg2+ for Mg2+ efflux and Na+ could leave the rat erythrocyte via this transport system. Na+/Mg2+ antiport was working asymmetrically with respect to extra- and intracellular Na+ and Mg2+, and did not perform net Mg2+ uptake.
  • |Adenosine Triphosphatases/metabolism[MESH]
  • |Adenosine Triphosphate/analysis/physiology[MESH]
  • |Amiloride/pharmacology[MESH]
  • |Animals[MESH]
  • |Biological Transport/drug effects[MESH]
  • |Erythrocyte Membrane/enzymology/metabolism[MESH]
  • |Erythrocytes/drug effects/*metabolism[MESH]
  • |Intracellular Membranes/analysis[MESH]
  • |Kinetics[MESH]
  • |Magnesium/*metabolism/physiology[MESH]
  • |Quinidine/pharmacology[MESH]
  • |Rats[MESH]
  • |Sodium/metabolism/*pharmacology[MESH]


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