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This Article Full Text Full Text (PDF) All Versions of this Article: 289/4/F742    most recent 00091.2005v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Web of Science (2) Citing Articles via Google Scholar Google Scholar Articles by Watanabe, M. Articles by Matsufuji, S. Search for Related Content PubMed PubMed Citation Articles by Watanabe, M. Articles by Matsufuji, S.

Enhanced sodium-dependent extrusion of magnesium in mutant cells established from a mouse renal tubular cell line

¹Department of Physiology, Tokyo Medical University, Tokyo, Japan; and ²Department of Biochemistry II and ³Division of Nephrology and Hypertension, The Jikei University School of Medicine, Tokyo, Japan

Submitted 7 March 2005 ; accepted in final form 7 May 2005

To study the regulatory mechanisms of intracellular Mg²⁺ concentration ([Mg²⁺]_i) in renal tubular cells as well as in other cell types, we established a mutant strain of mouse renal cortical tubular cells that can grow in culture media with very high extracellular Mg²⁺ concentrations ([Mg²⁺]_o > 100 mM: 101Mg-tolerant cells). [Mg²⁺]_i was measured with a fluorescent indicator furaptra (mag-fura 2) in wild-type and 101Mg-tolerant cells. The average level of [Mg²⁺]_i in the 101Mg-tolerant cells was kept lower than that in the wild-type cells either at 51 mM or 1 mM [Mg²⁺]_o. When [Mg²⁺]_o was lowered from 51 to 1 mM, the decrease in [Mg²⁺]_i was significantly faster in the 101Mg-tolerant cells than in the wild-type cells. These differences between the 101Mg-tolerant cells and the wild-type cells were abolished in the absence of extracellular Na⁺ or in the presence of imipramine, a known inhibitor of Na⁺/Mg²⁺ exchange. We conclude that Na⁺-dependent Mg²⁺ transport activity is enhanced in the 101Mg-tolerant cells. The enhanced Mg²⁺ extrusion may prevent [Mg²⁺]_i increase to higher levels and may be responsible for the Mg²⁺ tolerance.

membrane transport; sodium/magnesium exchange