Atrial Natriuretic Factor-Induced Amylase Output in the Rat Parotid Gland Appears to be Mediated by the Inositol Phosphate Pathway

BIANCIOTTI LG; VATTA MS; ELVERDIN J; DI CARLO MB; NEGRI G; FERNADEZ BE

BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS

ACADEMIC PRESS INC ELSEVIER SCIENCE

Año: 1998 vol. 247 p. 123 - 128

0006-291X

In previous in vivo studies we have reported that modulator of the biological responses of the digestiveatrial natriuretic factor enhanced induced salivary se- system. ANF modulates biliary, intestinal, pancreaticcretion and increased isoproterenol-induced amylase and salivary secretions as well as bowel motility in the release in the rat suggesting that, ANF effect could bemediated by phosphatidylinositol hydrolysis. In the rat (2?5). Although cGMP is the intracellular messenpresentwork, the effect of ANF on rat parotid tissue ger that mediates most of ANF biological effects, thisincubated in vitro was investigated with the aim to second messenger seems not to be involved in the efassesswhether the phosphoinositol pathway was in- fects of ANF on the digestive exocrine glands, in spitevolved in ANF intracellular signaling in the parotid of the finding that cGMP increases have been reportedgland. Results showed that ANF induced a dose depen- to occur upon ANF receptor stimulation in the pancreasdent increase in amylase fractional release, which was as well as the salivary glands (6,7). The finding oflower than that evoked by any concentration of isopro- mRNA ANF in the gastrointestinal tract and the digesterenol.Furthermore 100 nMANF enhanced isoproter- tive exocrine glands suggests local synthesis of the pepenol-evoked amylase release. The effect of ANF was tide and supports a paracrine role (8?10).not affected in the presence of propranolol suggesting We have previously reported that ANF was not athe noninvolvement of the b adrenergic receptor, sialogogic agonist at least in the concentrations tested,which is the main stimulus for the output of the en- although it enhanced the salivary secretion induced byzyme in the parotid gland. However, ANF increased different sialogogic agonists in rat. ANF potentiatedphosphatidylinositol hydrolysis, which implies an in- metacholine, methoxamine and substance P evokedcrease in intracellular calcium, which is necessary for salivation both in the parotid and submaxillary glandsthe achievement of maximal response in amylase re- (4). Furthermore, ANF also modified the electrolyte exlease.This effect was abolished in the presence of neo- cretion pattern induced by these sialogogic agonists mycin supporting ANF direct stimulation of phospho- lipase C. These results suggest the involvement of the (11). Coversely, when salivation was evoked by a bCtype natriuretic peptide receptor coupled to phos- adrenergic agonist such as isoproterenol, ANF did notpholipase C in ANF evoked amylase release and ANF modify the salivary flow, however it potentiated proteinenhancement of the isoproterenol-induced output of and amylase induced output (4,11).the enzyme.