Does cyclic GMP mediate amylase release from mouse parotid acini?
In mouse parotid acini both cholinergic and beta-adrenergic agonists increased intracellular levels of cyclic-GMP (c-GMP) as well as amylase release. The derivative of c-GMP, 8-bromo-c-GMP, mimicked the effects of cholinergic and beta-adrenergic stimulation on amylase release. Nitroprusside (NP), hydroxylamine (HA) and sodium azide (NaA) increased c-GMP levels and also enhanced amylase release in a dose-dependent manner; cyclic-AMP (c-AMP) levels were not affected. The phosphodiesterase inhibitor 3-isobutyl-1-methyl-xanthine (MIX) enhanced the effects of carbachol on both c-GMP accumulation and amylase release. These results suggest that c-GMP may mediate the actions of cholinergic agonists and at least partially mediate the actions of beta-adrenergic agonists on mouse parotid enzyme release.
D015056:1-Methyl-3-isobutylxanthine / Q000494:pharmacology; D000681:Amylases / Q000378:metabolism*; D000818:Animals; D001386:Azides / Q000494:pharmacology; D003994:Bucladesine / Q000494:pharmacology; D002217:Carbachol / Q000494:pharmacology; D006152:Cyclic GMP / Q000031:analogs & derivatives / Q000494:pharmacology / Q000502:physiology*; D006898:Hydroxylamines / Q000494:pharmacology; D051379:Mice; D009599:Nitroprusside / Q000494:pharmacology; D010306:Parotid Gland / Q000187:drug effects / Q000201:enzymology*; D019810:Sodium Azide
D001386:Azides; D006898:Hydroxylamines; D009599:Nitroprusside; C016276:8-bromocyclic GMP; D003994:Bucladesine; D002217:Carbachol; D019810:Sodium Azide; D000681:Amylases; D006152:Cyclic GMP; D015056:1-Methyl-3-isobutylxanthine