Magnesium reabsorption

Shafik, I. M., and Quamme, G. A. (1989). Early adaptation of renal magnesium reabsorption in response to magnesium restriction. Am. J. Physiol. 257, F974-F977. 

Hypernatremia may reduce magnesium reabsorption, but if sodium is lost with diuretics, magnesium reabsorption will not be reduced. 

While sodium reabsorption in the distal nephron, influenced by aldosterone, is particularly important because it can produce sodium-free urine and promote potassium loss, the great majority of renal sodium reabsorption occurs elsewhere about 25% in the loop of Henle and most in the proximal tubule. The loop is also a main site of magnesium reabsorption, hence the tendency for loop diuretics to cause hypomagnesemia. 

The nephronic parts of the kidney are the principal diuretic active sites for secreting ede-matic fluid from the organism. Diuretics basically increase secretion of water and salts from the kidneys by suppressing reabsorption of a few main ions (primarily sodium and chloride ions) however, secretion of calcium, potassium, magnesium, and hydrocarbonate ions also increases to some degree. 

This transporter is selectively blocked by diuretic agents known as "loop" diuretics (see later in chapter). Although the Na+/K+/2Cr transporter is itself electrically neutral (two cations and two anions are cotransported), the action of the transporter contributes to excess K+ accumulation within the cell. Back diffusion of this K+ into the tubular lumen causes a lumen-positive electrical potential that provides the driving force for reabsorption of cations—including magnesium and calcium—via the paracellular pathway. Thus, inhibition of salt transport in the TAL by loop diuretics, which reduces the lumen-positive potential, causes an increase in urinary excretion of divalent cations in addition to NaCI. 

The principal effects of calcitonin are to lower serum calcium and phosphate by actions on bone and kidney. Calcitonin inhibits osteoclastic bone resorption. Although bone formation is not impaired at first after calcitonin administration, with time both formation and resorption of bone are reduced. Thus, the early hope that calcitonin would prove useful in restoring bone mass has not been realized. In the kidney, calcitonin reduces both calcium and phosphate reabsorption as well as reabsorption of other ions, including sodium, potassium, and magnesium. Tissues other than bone... 

Parathyroid Hormone Parathyroid hormone raises plasma calcium by direct effects on bone resorption and renal reabsorption of calcium, and indirectly by regulating the metabolism of vitamin D. It is a peptide and acts via cell surface G-protein receptors linked to adenylate cyclase. The parathyroid glands have G-protein cell surface calcium receptors linked to phospholipase G, and parathyroid hormone is secreted in response to hypocalcemia. Magnesium is required for secretion of the hormone, which may explain the development of hypocalcemia in premature infants who are magnesium deficient. 

Renal magnesium wasting is the main mechanism responsible for the hypomagnesemia associated with cisplatin (172), and it can be associated with enhanced tubular reabsorption of calcium and consequent hypocalciuria (173). This dissociation in the renal handling of calcium and magnesium is similar to what is found in Bartter s syndrome. The site of the renal tubular defect in these conditions is not known, but there is evidence that active renal tubular transport systems are disrupted. 

As a consequence of the blockade of the Na, K, 2Cr-cotransporter, the diuresis produced by furosemide (frusemide) results in increased urinary excretion of sodium, potassium, chloride, calcium and magnesium ions. The losses of sodium, potassium and chloride are approximately 1750, 600 and 2150 mmol, respectively, after i.m. administration of furosemide (frusemide) at 1 mg/kg. Although these electrolyte losses are substantial, they are largely replaced (within the 24 h period following furosemide (frusemide) administration) by enhanced renal reabsorption as well increased ion absorption from the intestinal tract. In addition to this primary action, furosemide (frusemide) may have a lesser inhibitory effect on other chloride ion transporters and the drug can also inhibit carbonic anhydrase activity (Martinez-Maldonado Cordova 1990, Rose 1989,1991, Wilcox 1991). Finally, some of the renal and extrarenal effects of furosemide (frusemide) appear to be mediated through increased prostaglandin production. 

Loop or high-ceiling diuretics inhibit the transport of sodium in the ascending Loop of Henle and result in the excretion of sodium and water, potassium, calcium, and magnesium. Loop diuretics are more effective with inhibiting reabsorption of sodium than thiazides diuretics. 

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