CELLULAR AND PARACELLULAR MAGNESIUM TRANSPORT ACROSS THE TERMINAL ILEUM OF THE RAT AND ITS INTERACTION WITH THE CALCIUM-TRANSPORT

Concentration and voltage dependence of unidirectional magnesium fluxes across the stripped mucosa of the rat terminal ileum were measured in an Ussing chamber. The mucosa-to-serosa magnesium flux exhibited a curvilinear concentration dependence, whereas serosa-to-mucosa flux of magnesium was linearly related to magnesium concentration between 0.25 and 5 mM. At low concentrations magnesium was absorbed, whereas at the magnesium concentration of 5 mM the serosa-to-mucosa magnesium flux was higher than the mucosa-toserosa flux, resulting in magnesium secretion. Only the mucosa-to-serosa flux of magnesium had a voltage-independent (i.e., nondiffusive) cellular component. Due to the high capacity of this cellular mucosa-to-serosa transport of magnesium, which was about 7.5 times greater than that of calcium, absorption of magnesium was performed in the terminal ileum in contrast to calcium, which was secreted under the same conditions. However, magnesium serosa-to-mucosa flux was totally voltage dependent (i.e., diffusive) and probably restricted to the paracellular pathway. The diffusive serosa-to-mucosa flux of magnesium was about two times greater than the diffusive fraction of the mucosa-to-serosa transport of magnesium. The prevalence of the diffusive serosa-to-mucosa flux of magnesium over that from mucosa to serosa, responsible for magnesium secretion observed at the magnesium concentration of 5 mM, may be explained by an "anomalous solvent drag effect." Voltage clamp experiments showed that magnesium had no effect on the cellular mucosa-to-serosa transport of calcium. However, it decreased the diffusive calcium flux in this direction. 1α,25-dihydroxyvitamin D3, did not influence the unidirectional or net magnesium transport but increased the calcium flux in both directions to the same degree. In conclusion, magnesium is absorbed in the terminal ileum at least partially by a cellular, vitamin D3-insensitive process that is different from the calcium transport mechanism. © 1990.