C-type natriuretic peptide stimulates pancreatic exocrine secretion in the rat: Role of vagal afferent and efferent pathways.

SABBATINI M; RODRIGUEZ M; DABAS P; VATTA MS; BIANCIOTTI LG

EUROPEAN JOURNAL OF PHARMACOLOGY

Elsevier

Lugar: Amsterdam; Año: 2007 vol. 577 p. 192 - 202

0014-2999

We previously reported that centrally applied C-type natriuretic peptide (CNP) enhances pancreatic exocrine secretion through vagal pathways mediated by the activation of natriuretic peptide receptors A and/or B in the brain. In the present study we sought to establish whether CNP was involved in the peripheral regulation of pancreatic exocrine secretion. Anesthetized rats were prepared with pancreatic duct cannulation, pyloric ligation and bile diversion into the duodenum. CNP dose-dependently enhanced pancreatic flow, chloride and protein excretion but did not modify bicarbonate output. A selective natriuretic peptide receptor C agonist enhanced pancreatic flow and mimicked CNP-evoked protein output but failed to modify chloride secretion. Truncal vagotomy and hexamethonium pretreatment reduced CNP-evoked pancreatic flow and abolished chloride excretion but did not affect protein output. Perivagal application of capsaicin induced similar results. Furthermore pretreatment with atropine reduced pancreatic flow and chloride excretion but failed to modify protein output. Partial muscarinic blockade of CNP-evoked chloride output suggested that mediators others than acetylcholine were involved. However CNP response was unaltered by cholecystokinin and vasoactive intestinal peptide receptor blockade or by nitric oxide synthase inhibition. In conclusion, CNP stimulated pancreatic flow through natriuretic peptide receptor C and the vago-vagal reflex but it increased protein output only by natriuretic peptide receptor C activation and chloride excretion by vago-vagal reflexes. This study supports that CNP is involved in the complex neuronal, hormonal and peptidergic regulation of pancreatic exocrine secretion in the rat.