title: Atrial natriuretic factor-induced amylase output in the rat parotid gland appears to be mediated by the inositol phosphate pathway.
abstract: In previous in vivo studies we have reported that atrial natriuretic factor enhanced induced salivary secretion and increased isoproterenol-induced amylase release in the rat suggesting that, ANF effect could be mediated by phosphatidylinositol hydrolysis. In the present work, the effect of ANF on rat parotid tissue incubated in vitro was investigated with the aim to assess whether the phosphoinositol pathway was involved in ANF intracellular signaling in the parotid gland. Results showed that ANF induced a dose dependent increase in amylase fractional release, which was lower than that evoked by any concentration of isoproterenol. Furthermore 100 nM ANF enhanced isoproterenol-evoked amylase release. The effect of ANF was not affected in the presence of propranolol suggesting the noninvolvement of the beta adrenergic receptor, which is the main stimulus for the output of the enzyme in the parotid gland. However, ANF increased phosphatidylinositol hydrolysis, which implies an increase in intracellular calcium, which is necessary for the achievement of maximal response in amylase release. This effect was abolished in the presence of neomycin supporting ANF direct stimulation of phospholipase C. These results suggest the involvement of the C type natriuretic peptide receptor coupled to phospholipase C in ANF evoked amylase release and ANF enhancement of the isoproterenol-induced output of the enzyme.
authors.affiliation: Cátedras de Fisiología, Facultad de Farmacia y Bioquímica, Universidad de Buenos Aires, Argentina.
authors.forename: L G
authors.initials: LG
authors.lastname: Bianciotti
authors.forename: M S
authors.initials: MS
authors.lastname: Vatta
authors.forename: J C
authors.initials: JC
authors.lastname: Elverdin
authors.forename: M B
authors.initials: MB
authors.lastname: di Carlo
authors.forename: G
authors.initials: G
authors.lastname: Negri
authors.forename: B E
authors.initials: BE
authors.lastname: Fernandez
mesh_terms: D000318:Adrenergic beta-Agonists / Q000494:pharmacology; D000681:Amylases / Q000187:drug effects / Q000378:metabolism*; D000818:Animals; D009320:Atrial Natriuretic Factor / Q000502:physiology*; D006152:Cyclic GMP / Q000031:analogs & derivatives / Q000494:pharmacology; D004357:Drug Synergism; D007295:Inositol Phosphates / Q000502:physiology*; D007545:Isoproterenol / Q000494:pharmacology; D008297:Male; D010306:Parotid Gland / Q000187:drug effects / Q000201:enzymology*; D010716:Phosphatidylinositols / Q000378:metabolism; D011433:Propranolol / Q000494:pharmacology; D051381:Rats; D017208:Rats, Wistar
chemical_list: D000318:Adrenergic beta-Agonists; D007295:Inositol Phosphates; D010716:Phosphatidylinositols; C472610:atrial natriuretic peptide, rat; C016276:8-bromocyclic GMP; D009320:Atrial Natriuretic Factor; D011433:Propranolol; D000681:Amylases; D006152:Cyclic GMP; D007545:Isoproterenol