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Am J Physiol Gastrointest Liver Physiol 280: G1145-G1156, 2001;
0193-1857/01 $5.00
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Vol. 280, Issue 6, G1145-G1156, June 2001

alpha 1-Adrenoceptor-induced Mg2+ extrusion from rat hepatocytes occurs via Na+-dependent transport mechanism

Theresa E. Fagan and Andrea Romani

Department of Physiology and Biophysics, School of Medicine, Case Western Reserve University, Cleveland, Ohio 44106-4970

The stimulation of the alpha 1-adrenergic receptor by phenylephrine results in a sizable extrusion of Mg2+ from liver cells. Phenylephrine-induced Mg2+ extrusion is almost completely abolished by the removal of extracellular Ca2+ or in the presence of SKF-96365, an inhibitor of capacitative Ca2+ entry. In contrast, Mg2+ extrusion is only partially inhibited by the Ca2+-channel blockers verapamil, nifedipine, or (+)BAY-K8644. Furthermore, Mg2+ extrusion is almost completely prevented by TMB-8 (a cell-permeant inhibitor of the inositol trisphosphate receptor), 1,2-bis(2-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid (an intracellular Ca2+-chelating agent), or W-7 (a calmodulin inhibitor) Thapsigargin can mimic the effect of phenylephrine, and the coaddition of thapsigargin and phenylephrine does not result in an enlarged extrusion of Mg2+ from the hepatocytes. Regardless of the agonist used, Mg2+ extrusion is inhibited by >90% when hepatocytes are incubated in the presence of physiological Ca2+ but in the absence of extracellular Na+. Together, these data suggest that the stimulation of the hepatic alpha 1-adrenergic receptor by phenylephrine results in an extrusion of Mg2+ through a Na+-dependent pathway and a Na+-independent pathway, both activated by changes in cellular Ca2+.

alpha 1-adrenergic receptor; magnesium homeostasis


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