Effect of sodium ions on cyclic AMP and cyclic GMP levels in mouse parotid acini.
The ability of the beta-adrenergic agonist, isoproterenol, to elevate intracellular levels of cyclic-AMP (c-AMP) and cyclic GMP (c-GMP) in mouse parotid acini was dependent upon the extracellular sodium concentration. In the absence of extracellular sodium isoproterenol-stimulated c-GMP and c-AMP levels were significantly reduced; carbachol-stimulated c-GMP levels were not affected. Monensin, a sodium ionophore, mimicked the effects of isoproterenol in elevating c-GMP levels; this effect was abolished in the absence of extracellular sodium. Monensin did not mimic the effects of isoproterenol in elevating c-AMP levels. The data presented suggests that sodium ions may play a role in beta-adrenergic regulation of cyclic nucleotide levels in mouse parotid gland and that the mechanisms involved in regulation of c-AMP and c-GMP levels appear to be different.
D000318:Adrenergic beta-Agonists; D000818:Animals; D000001:Calcimycin / Q000494:pharmacology; D002217:Carbachol / Q000494:pharmacology; D000242:Cyclic AMP / Q000378:metabolism*; D006152:Cyclic GMP / Q000378:metabolism*; D007545:Isoproterenol / Q000494:pharmacology*; D007700:Kinetics; D051379:Mice; D008985:Monensin / Q000494:pharmacology; D010306:Parotid Gland / Q000378:metabolism*; D012964:Sodium / Q000502:physiology*
D000318:Adrenergic beta-Agonists; D000001:Calcimycin; D002217:Carbachol; D008985:Monensin; D012964:Sodium; D000242:Cyclic AMP; D006152:Cyclic GMP; D007545:Isoproterenol