Watson E L, Dowd F
Eur J Pharmacol. 1983 Mar 25;88(2-3):153-60. doi: 10.1016/0014-2999(83)90001-8.
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.
