ArticleMolecular and cellular biochemistry2011
Modulation of Na+/Mg²+ exchanger stoichiometry ratio by Cl⁻ ions in basolateral rat liver plasma membrane vesicles.
Article in Molecular and cellular biochemistry, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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1 citing paper in PubMed, 5 citations in OpenAlex.
- Cellular magnesium homeostasis.Archives of biochemistry and biophysics · 2011Review
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Abstract
The Na+/Mg²+ exchanger represents the main Mg²+ extrusion mechanism operating in mammalian cells including hepatocytes. We have previously reported that this exchanger, located in the basolateral domain of the hepatocyte, promotes the extrusion of intravesicular trapped Mg²+ for extravesicular Na+ with ratio 1. This electrogenic exchange is supported by the accumulation of tetraphenyl-phosphonium within the vesicles at the time when Mg²+ efflux occurs. In this present study, the role of extra- and intra-vesicular Cl⁻ on the Na+/Mg²+ exchange ratio was investigated. The results reported here suggest that Cl⁻ ions are not required for the Na+ to Mg²+ exchange to occur, but the stoichiometry ratio of the exchanger switches from electrogenic (1Na(in)+ :1Mg(out)²+) in the presence of intravesicular Cl⁻ to electroneutral (2Na(in)+ :1 Mg(out)²+) in their absence. In basolateral liver plasma membrane vesicles loaded with MgCl₂ labeled with ³⁶Cl⁻, a small but significant Cl⁻ efflux (~30 nmol Cl⁻/mg protein/1 min) is observed following addition of NaCl or Na-isethionate to the extravesicular medium. Both Cl⁻ and Mg²+ effluxes are inhibited by imipramine but not by amiloride, DIDS, niflumic acid, bumetanide, or furosemide. In vesicles loaded with Mg-gluconate and stimulated by Na-isethionate, an electroneutral Mg²+ extrusion is observed. Taken together, these results suggest that the Na+/Mg²+ exchanger can operate irrespective of the absence or the presence of Cl⁻ in the extracellular or intracellular environment. Changes in trans-cellular Cl⁻ content, however, can affect the modus operandi of the Na+/Mg²+ exchanger, and consequently impact "cellular" Na+ and Mg²+ homeostasis as well as the hepatocyte membrane potential.
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