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Division of Nephrology, Department of Medicine, School of Medicine, University of California San Diego, La Jolla, California.
Correspondence to Dr. Darrell D. Fanestil, Department of Medicine 0623B, University of California, San Diego, 9500 Gilman Drive, La Jolla, CA 92093-0623. Phone: 619-534-4164; Fax: 619-534-1424; E-mail: dfanestil{at}ucsd.edu
Abstract. This study reports for the first time a relationship between dietary Mg and the renal thiazide-sensitive Na-Cl cotransporter (TZR, measured by saturation binding with 3H-metolazone). Ion-selective electrodes measured plasma ionized magnesium (PMg+ +), calcium (PCa + +), and potassium (PK +). Restricting dietary Mg for 1 wk decreased PMg + + 18%, TZR 25%, and renal excretion of magnesium (UMg) and calcium (UCa) more than 50% without changing PCa + +, PK +, or plasma aldosterone. A low Mg diet for 1 d significantly decreased PMg + +, TZR, UMg and UCa. Return of dietary Mg after 5 d of Mg restriction restored PMg + + and TZR toward normal. In the control, Mg-deficient, and Mg-repleting animals, TZR correlated with PMg + + (r = 0.86) and with UMg (r = 0.87) but not UCa (r = 0.09). Increasing oral intake of Mg for 1 wk increased PMg + + 14%, TZR 32%, UMg 74%, and UCa more than fourfold without changing PCa + + or PK +. In contrast, increasing dietary Ca content from 0.02% to 1.91% did not change TZR, but increased UCa fivefold without changing PCa + +. Hormonal mediators (if any) involved in the relationship between dietary Mg and TZR remain to be elucidated, as does the relationship between TZR and tubular reabsorption of Mg.
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