Dietary magnesium, not calcium, regulates renal thiazide receptor

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 (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.