Activation of Na + - and Ca 2+ -dependent Mg 2+ extrusion by α 1 - and β-adrenergic agonists in rat liver cells

• Published in: American journal of physiology: Gastrointestinal and liver physiology 2000-11, Vol.279 (5), p.G943-G950
• Main Authors: Fagan, Theresa E., Romani, Andrea
• Format: Article
• Language: English
• ISSN: 0193-1857; 1522-1547
• DOI: 10.1152/ajpgi.2000.279.5.G943

The administration of selective α 1 (phenylephrine)-, β (isoproterenol)-, or mixed (epinephrine) adrenergic agonists induces a marked Mg 2+ extrusion from perfused rat livers. In the absence of extracellular Ca 2+ , phenylephrine does not induce a detectable Mg 2+ extrusion, isoproterenol-induced Mg 2+ mobilization is unaffected, and epinephrine induces a net Mg 2+ extrusion that is lower than in the presence of extracellular Ca 2+ and quantitatively similar to that elicited by isoproterenol. In the absence of extracellular Na + , no Mg 2+ is extruded from the liver irrespective of the agonist used. Similar results are observed in perfused livers stimulated by glucagon or 8-chloroadenosine 3′,5′-cyclic monophosphate. In the absence of extracellular Na + or Ca 2+ , adrenergic-induced glucose extrusion from the liver is also markedly decreased. Together, these results indicate that liver cells extrude Mg 2+ primarily via a Na + -dependent mechanism. This extrusion pathway can be activated by the increase in cellular cAMP that follows the stimulation by glucagon or a specific β-adrenergic receptor agonist or, alternatively, by the changes in cellular Ca 2+ induced by the stimulation of the α 1 -adrenoceptor. In addition, the stimulation of the α 1 -adrenoceptor appears to activate an auxiliary Ca 2+ -dependent Mg 2+ extrusion pathway. Finally, our data suggest that experimental conditions that affect Mg 2+ mobilization also interfere with glucose extrusion from liver cells.