Activation of Na(+)- and Ca(2+)-dependent Mg(2+) extrusion by alpha(1)- and beta-adrenergic agonists in rat liver cells.
Am J Physiol Gastrointest Liver Physiol
; 279(5): G943-50, 2000 Nov.
Article
en En
| MEDLINE
| ID: mdl-11052991
ABSTRACT
The administration of selective alpha(1) (phenylephrine)-, beta (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 beta-adrenergic receptor agonist or, alternatively, by the changes in cellular Ca(2+) induced by the stimulation of the alpha(1)-adrenoceptor. In addition, the stimulation of the alpha(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.
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Colección:
01-internacional
Base de datos:
MEDLINE
Asunto principal:
Sodio
/
8-Bromo Monofosfato de Adenosina Cíclica
/
Calcio
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Receptores Adrenérgicos beta
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Receptores Adrenérgicos alfa 1
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Hepatocitos
/
Magnesio
Límite:
Animals
Idioma:
En
Revista:
Am J Physiol Gastrointest Liver Physiol
Asunto de la revista:
FISIOLOGIA
/
GASTROENTEROLOGIA
Año:
2000
Tipo del documento:
Article
País de afiliación:
Estados Unidos