cAMP activates magnesium efflux via the Na/Mg antiporter in ascites cells.
In intact ascites cells magnesium efflux is substantially stimulated by cAMP analogues and by low concentrations of prostaglandins (PGE1 and PGE2) which increases the synthesis of cAMP. cAMP stimulates magnesium efflux by directly stimulating the Na-Mg antiporter rather than determining a magnesium release from mitochondria as reported for other cell types. Protein kinase inhibitors abolish the cAMP stimulated magnesium efflux suggesting that the stimulation is mediated by the phosphorylation of the carrier protein, increasing its affinity for intracellular magnesium. These data provide evidence that receptor-mediated stimuli eventually leading to cell activation are directly connected to the regulation of intracellular magnesium.
Wolf
F I
FI
Institute of General Pathology, Catholic University School of Medicine, Roma, Italy.
Di Francesco
A
A
Covacci
V
V
Cittadini
A
A
D000818:Animals; D017920:Antiporters / Q000187:drug effects* / Q000378:metabolism; D001692:Biological Transport; D002286:Carcinoma, Ehrlich Tumor / Q000378:metabolism* / Q000473:pathology; D000242:Cyclic AMP / Q000494:pharmacology*; D008274:Magnesium / Q000378:metabolism*; D051379:Mice; D010766:Phosphorylation; D012964:Sodium / Q000378:metabolism; D014407:Tumor Cells, Cultured
D017920:Antiporters; C046250:sodium-magnesium antiporter; D012964:Sodium; D000242:Cyclic AMP; D008274:Magnesium