Diphenylhydantoin: effects on amylase release, cyclic nucleotides and ion fluxes in mouse parotid acini.
The effects of diphenylhydantoin were investigated on isolated mouse parotid acini. Diphenylhydantoin inhibited carbachol-stimulated amylase release at concentrations of 5 X 10(-4) M and greater; isoproterenol-stimulated amylase release was not affected. The inhibition of carbachol-stimulated amylase release was attributable to inhibition of 45Ca2+ uptake. The ability of diphenylhydantoin to inhibit carbachol-stimulated cyclic GMP (c-GMP) accumulation was also related to inhibition of 45Ca2+ uptake. Diphenylhydantoin (5 X 10(-4)M) alone, was found to stimulate c-GMP accumulation, an effect related to enhanced 45Ca2+ efflux. Diphenylhydantoin alone, however, failed to enhance amylase release. These findings suggest that the effects of diphenylhydantoin on carbachol-stimulated amylase release and on c-GMP accumulation are related to its effects on transmembrane calcium movements.
D000681:Amylases / Q000378:metabolism*; D000818:Animals; D002118:Calcium / Q000378:metabolism*; D002217:Carbachol / Q000494:pharmacology; D000242:Cyclic AMP / Q000378:metabolism*; D006152:Cyclic GMP / Q000378:metabolism*; D066298:In Vitro Techniques; D051379:Mice; D010306:Parotid Gland / Q000187:drug effects* / Q000378:metabolism; D010672:Phenytoin / Q000494:pharmacology*; D012964:Sodium / Q000378:metabolism*
D010672:Phenytoin; D002217:Carbachol; D012964:Sodium; D000242:Cyclic AMP; D000681:Amylases; D006152:Cyclic GMP; D002118:Calcium