Effects of acute metabolic acid-base changes and furosemide on magnesium excretion in rats

Abstract

The effect of acute metabolic acid-base changes on renal magnesium transport is not well defined. We have examined renal magnesium handling in three groups of ten acutely thyroparathyroidectomized rats infused with isotonic NaCl (controls), NH 4Cl (acidosis), and NaHCO 3 (alkalosis). To define the interactions of furosemide with acid-base changes and in an attempt to localize the site of action of acidosis and alkalosis on tubular magnesium transport, the rats were studied in a second phase after administration of a maximal dose of furosemide. Before furosemide, the blood pH was 7.40 in the controls, 7.27 ( P < 0.001) in the acidotic rats, and 7.56 ( P < 0.001) in the alkalotic rats. The filtered magnesium load was not significantly different in the three groups, but fractional excretion of magnesium (FEMg) was 33.7%, 37.4%, and 13.3% in the controls, the acidosis group, and the alkalosis group, respectively. Following furosemide, the blood pH was unchanged in each group, but FEMg increased significantly to 55.4%, 71.1% ( P < 0.01 compared with controls), and 41.4% ( P < 0.01 compared with controls) in the controls, the acidotic rats, and the alkalotic rats, respectively. These data indicate that metabolic alkalosis per se enhances renal magnesium transport, and this effect is also evident after blockade of loop magnesium reabsorption by a maximal dose of furosemide. Acidosis per se does not significantly alter magnesium transport, but an inhibitory effect of acidosis on magnesium reabsorption becomes evident when distal magnesium delivery is greatly increased by furosemide. These interactions suggest that metabolic acid-base changes and furosemide may influence magnesium reabsorption at different tubule sites. We propose that, in accord with recent micropuncture studies, metabolic alkalosis may enhance magnesium reabsorption in the descending limb of Henle's loop, probably the pars recta, while metabolic acidosis may have an inhibitory effect on magnesium reabsorption that is located in the distal tubule.