INVESTIGADORES
VATTA Marcelo Sergio
artículos
Título:
Atrial natriuretic factor intracellular signaling in the rat submandibular gland
Autor/es:
VENTIMIGLIA M; RODRIGUEZ M; ELVERDIN J; DAVIO C; VATTA MS; BIANCIOTTI LG
Revista:
REGULATORY PEPTIDES
Editorial:
ELSEVIER SCIENCE BV
Referencias:
Lugar: AMSTERDAM; Año: 2008 vol. 150 p. 43 - 49
ISSN:
0167-0115
Resumen:
Atrial natriuretic factor intracellular signaling in the rat submandibular gland
María S. Ventimiglia a, Myrian R. Rodríguez a, Juan C. Elverdín b, Carlos A. Davio c,
Marcelo S. Vatta d, Liliana G. Bianciotti a
Abstract
We previously reported that intravenously administered atrial natriuretic factor (ANF) induced no salivation but enhanced agonist-evoked secretion in submandibular glands. The gene expression of ANF and natriuretic peptide receptors (NPR) was later reported in the glands. In the present study we sought to establish the intracellular signalling mechanisms underlying ANF modulation of salivary secretion. Fasted rats were prepared with submandibular duct and femoral cannulation. Doseresponse curves to methacholine (MC) and norepinephrine (NE) were performed in the presence of cANP (423 amide) (selective NPR-C agonist) and ANF. Local injection of the agonist or ANF-induced no salivation, but enhanced MC and NE-evoked secretion. ANF and cANP (423 amide) enhanced phosphoinositide turnover being the effect abolished by U73122 (PLC inhibitor). Further ANF and cANP (423 amide) decreased basal cAMP content but failed to affect isoproterenol or forskolin-evoked cAMP. ANF response was inhibited by pertussis toxin and mimicked by cANP (423 amide) strongly supporting NPR-C activation. ANF-induced cAMP reduction was abolished by
PLC and PKC inhibitors. The content of cGMP was dose dependently stimulated by ANF but not modified by cANP (423 amide). These findings support that ANF through NPR-C receptors coupled to PLC activation and adenylyl cyclase inhibition interacts with sialogogic agonists in the submandibular gland to potentiate salivation.