Abstract
Collagenase dispersed rat liver hepatocytes release Mg2+ when stimulated with norepinephrine or accumulate Mg2+ when stimulated with vasopressin, respectively. Mg2+ fluxes in either direction account for a net loss or gain of approximately 10% of total cell magnesium and are rapidly reversible. Both stimulated Mg2+ efflux and Mg2+ influx require physiological concentration of extracellular NaCl and Ca2+. In the absence of extracellular Na+, Mg2+ efflux, but not influx, can be observed in the presence of extracellular Cl-. Under these conditions, the efflux is inhibited by the Cl-/HCO3- exchanger inhibitor 4,4'-dinitrostilbene-2,2'-disulfonic acid. In hepatocytes, Mg2+ influx, but not efflux, is completely inhibited by thapsigargin, a specific inhibitor of the endoplasmic reticulum Ca2+ ATPase. Several lines of evidence, such as measurements of cytosolic Ca2+ or of cytosolic Ca2+ buffering, indicate that the effect of thapsigargin in inhibiting Mg2+ influx could not be explained by an increase in cytosolic Ca2+. Instead, the inhibition of hepatocyte Mg2+ influx was found to be the result of the depletion of the Ca2+ stored within the endoplasmic reticulum.
Highlights
Collagenase dispersed rat liver hepatocytes release Mg2+ when stimulated with norepinephrine or accumulate Mg2+ when stimulated with vasopressin, respectively
Several lines of evidence, such as measurements of cytosolic Ca2+ or of cytosolic Ca2+buffering, indicate that the effect of thapsigargin in inhibiting Mg2+influx could not be explained by an increase in cytosolic Ca2+.Instead, the inhibition of hepatocyte Mg2+ influxwas found to be the result of the depletion of the Ca2+stored within the endoplasmic reticulum
In this study,we investigated the role of extracellular Na+, and of other cations, in regulating Mg2+ efflux and Mg2' influx in liver cells
Summary
Collagenase dispersed rat liver hepatocytes release Mg2+ when stimulated with norepinephrine or accumulate Mg2+ when stimulated with vasopressin, respectively. M 6 + fluxes in eitherdirection account for a net loss or gain of approximately 10% of total cell magnesium and are rapidly reversible Both stimulated Mg2+efflux and Mgz+influx require physiological concentration of extracellular NaCl and Caz+.In the absence of extracellular Na+,Mg2+efflux, but not influx, can be observed in the presence of extracellular C1-. A large number of recent observations have shown that under physiological (5-8) and pathological (9-13) conditions, a major redistribution of Mg2' across cells and organelles occurs in liver (14-19), heart (5, 12, 18-20), and other tissues (6,21, 22) This and other laboratories have shown that a netMg2+efflux can be induced in perfused organs or isolated cells upon noradrenergic stimulation andconsequent increase in cell cAMP (18, 19). Evidence is provided that the endoplasmic reticulum, andits Ca2+storage properties within hepatocytes, is necessary for the observed stimulated M$+ influx but not M e efflux
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