Dietary Magnesium, Not Calcium, Regulates Renal Thiazide Receptor

. 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 3 H-metolazone). Ion-selective electrodes measured plasma ionized magnesium (P Mg + +), calcium (P Ca + +), and potassium (P K +). Restricting dietary Mg for 1 wk decreased P Mg + + 18%, TZR 25%, and renal excretion of magnesium (U Mg ) and calcium (U Ca ) more than 50% without changing P Ca + +, P K +, or plasma aldosterone. A low Mg diet for 1 d significantly decreased P Mg + +, TZR, U Mg and U Ca . Return of dietary Mg after 5 d of Mg restriction restored P Mg + + and TZR toward normal. In the control, Mg-deficient, and Mg-repleting animals, TZR correlated with P Mg + + ( r = 0.86) and with U Mg ( r = 0.87) but not U Ca ( r = 0.09). Increasing oral intake of Mg for 1 wk increased P Mg + + 14%, TZR 32%, U Mg 74%, and U Ca more than fourfold without changing P Ca + + or P K +. In contrast, increasing dietary Ca content from 0.02% to 1.91% did not change TZR, but increased U Ca fivefold without changing P Ca + +. 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.