Magnesium transport in the renal distal convoluted tubule

Physiol Rev. 2001 Jan;81(1):51-84. doi: 10.1152/physrev.2001.81.1.51.


The distal tubule reabsorbs approximately 10% of the filtered Mg(2+), but this is 70-80% of that delivered from the loop of Henle. Because there is little Mg(2+) reabsorption beyond the distal tubule, this segment plays an important role in determining the final urinary excretion. The distal convoluted segment (DCT) is characterized by a negative luminal voltage and high intercellular resistance so that Mg(2+) reabsorption is transcellular and active. This review discusses recent evidence for selective and sensitive control of Mg(2+) transport in the DCT and emphasizes the importance of this control in normal and abnormal renal Mg(2+) conservation. Normally, Mg(2+) absorption is load dependent in the distal tubule, whether delivery is altered by increasing luminal Mg(2+) concentration or increasing the flow rate into the DCT. With the use of microfluorescent studies with an established mouse distal convoluted tubule (MDCT) cell line, it was shown that Mg(2+) uptake was concentration and voltage dependent. Peptide hormones such as parathyroid hormone, calcitonin, glucagon, and arginine vasopressin enhance Mg(2+) absorption in the distal tubule and stimulate Mg(2+) uptake into MDCT cells. Prostaglandin E(2) and isoproterenol increase Mg(2+) entry into MDCT cells. The current evidence indicates that cAMP-dependent protein kinase A, phospholipase C, and protein kinase C signaling pathways are involved in these responses. Steroid hormones have significant effects on distal Mg(2+) transport. Aldosterone does not alter basal Mg(2+) uptake but potentiates hormone-stimulated Mg(2+) entry in MDCT cells by increasing hormone-mediated cAMP formation. 1,25-Dihydroxyvitamin D(3), on the other hand, stimulates basal Mg(2+) uptake. Elevation of plasma Mg(2+) or Ca(2+) inhibits hormone-stimulated cAMP accumulation and Mg(2+) uptake in MDCT cells through activation of extracellular Ca(2+)/Mg(2+)-sensing mechanisms. Mg(2+) restriction selectively increases Mg(2+) uptake with no effect on Ca(2+) absorption. This intrinsic cellular adaptation provides the sensitive and selective control of distal Mg(2+) transport. The distally acting diuretics amiloride and chlorothiazide stimulate Mg(2+) uptake in MDCT cells acting through changes in membrane voltage. A number of familial and acquired disorders have been described that emphasize the diversity of cellular controls affecting renal Mg(2+) balance. Although it is clear that many influences affect Mg(2+) transport within the DCT, the transport processes have not been identified.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Acid-Base Equilibrium / physiology
  • Aminoglycosides / toxicity
  • Animals
  • Antibiotics, Antineoplastic / toxicity
  • Cisplatin / toxicity
  • Diuretics / pharmacology
  • Hormones / metabolism
  • Hormones / pharmacology
  • Humans
  • Immunosuppressive Agents / toxicity
  • Ion Transport / drug effects
  • Ion Transport / physiology
  • Kidney Tubules, Distal / cytology
  • Kidney Tubules, Distal / drug effects
  • Kidney Tubules, Distal / metabolism*
  • Magnesium / metabolism*
  • Phosphates / deficiency
  • Phosphates / metabolism
  • Potassium Deficiency / metabolism
  • Receptors, Calcium-Sensing
  • Receptors, Cell Surface / metabolism
  • Renal Tubular Transport, Inborn Errors / metabolism


  • Aminoglycosides
  • Antibiotics, Antineoplastic
  • Diuretics
  • Hormones
  • Immunosuppressive Agents
  • Phosphates
  • Receptors, Calcium-Sensing
  • Receptors, Cell Surface
  • Magnesium
  • Cisplatin