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

María E. Sabbatini, Myrian R. Rodríguez, Paula Dabas, Marcelo S. Vatta, Liliana G. Bianciotti

Research output: Contribution to journalArticle

9 Citations (Scopus)

Abstract

We previously reported that C-type natriuretic peptide (CNP) increases amylase release in isolated pancreatic acini through natriuretic peptide receptor C activation and enhances pancreatic exocrine secretion via vagal pathways when applied to the brain. In the present study we sought to establish whether CNP was involved in the peripheral regulation of pancreatic 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, perivagal application of capsaicin and hexamethonium reduced CNP-evoked pancreatic flow and abolished chloride excretion but did not affect protein output. Furthermore, pre-treatment with atropine reduced both CNP-stimulated pancreatic flow and chloride excretion but failed to modify protein excretion. Partial muscarinic blockade of CNP-evoked chloride output suggested that mediators other 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 the activation of the 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. Present results suggest that CNP may play a role as a local regulator of the exocrine pancreas.

Original languageEnglish (US)
Pages (from-to)192-202
Number of pages11
JournalEuropean Journal of Pharmacology
Volume577
Issue number1-3
DOIs
StatePublished - Dec 22 2007

Fingerprint

C-Type Natriuretic Peptide
Afferent Pathways
Efferent Pathways
Chlorides
Proteins
Reflex
Vasoactive Intestinal Peptide Receptors
Truncal Vagotomy
Exocrine Pancreas
Hexamethonium
Pancreatic Ducts
Capsaicin
Cholecystokinin
Amylases
Bicarbonates
Atropine
Duodenum
Bile
Nitric Oxide Synthase
Catheterization

Keywords

  • Natriuretic peptide
  • Natriuretic peptide receptor C
  • Pancreatic exocrine secretion
  • Vago-vagal reflex

ASJC Scopus subject areas

  • Pharmacology

Cite this

C-type natriuretic peptide stimulates pancreatic exocrine secretion in the rat : Role of vagal afferent and efferent pathways. / Sabbatini, María E.; Rodríguez, Myrian R.; Dabas, Paula; Vatta, Marcelo S.; Bianciotti, Liliana G.

In: European Journal of Pharmacology, Vol. 577, No. 1-3, 22.12.2007, p. 192-202.

Research output: Contribution to journalArticle

Sabbatini, María E. ; Rodríguez, Myrian R. ; Dabas, Paula ; Vatta, Marcelo S. ; Bianciotti, Liliana G. / C-type natriuretic peptide stimulates pancreatic exocrine secretion in the rat : Role of vagal afferent and efferent pathways. In: European Journal of Pharmacology. 2007 ; Vol. 577, No. 1-3. pp. 192-202.
@article{511bf49b47c64e4cbdbf9fdb6531560e,
title = "C-type natriuretic peptide stimulates pancreatic exocrine secretion in the rat: Role of vagal afferent and efferent pathways",
abstract = "We previously reported that C-type natriuretic peptide (CNP) increases amylase release in isolated pancreatic acini through natriuretic peptide receptor C activation and enhances pancreatic exocrine secretion via vagal pathways when applied to the brain. In the present study we sought to establish whether CNP was involved in the peripheral regulation of pancreatic 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, perivagal application of capsaicin and hexamethonium reduced CNP-evoked pancreatic flow and abolished chloride excretion but did not affect protein output. Furthermore, pre-treatment with atropine reduced both CNP-stimulated pancreatic flow and chloride excretion but failed to modify protein excretion. Partial muscarinic blockade of CNP-evoked chloride output suggested that mediators other 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 the activation of the 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. Present results suggest that CNP may play a role as a local regulator of the exocrine pancreas.",
keywords = "Natriuretic peptide, Natriuretic peptide receptor C, Pancreatic exocrine secretion, Vago-vagal reflex",
author = "Sabbatini, {Mar{\'i}a E.} and Rodr{\'i}guez, {Myrian R.} and Paula Dabas and Vatta, {Marcelo S.} and Bianciotti, {Liliana G.}",
year = "2007",
month = "12",
day = "22",
doi = "10.1016/j.ejphar.2007.08.043",
language = "English (US)",
volume = "577",
pages = "192--202",
journal = "European Journal of Pharmacology",
issn = "0014-2999",
publisher = "Elsevier",
number = "1-3",

}

TY - JOUR

T1 - C-type natriuretic peptide stimulates pancreatic exocrine secretion in the rat

T2 - Role of vagal afferent and efferent pathways

AU - Sabbatini, María E.

AU - Rodríguez, Myrian R.

AU - Dabas, Paula

AU - Vatta, Marcelo S.

AU - Bianciotti, Liliana G.

PY - 2007/12/22

Y1 - 2007/12/22

N2 - We previously reported that C-type natriuretic peptide (CNP) increases amylase release in isolated pancreatic acini through natriuretic peptide receptor C activation and enhances pancreatic exocrine secretion via vagal pathways when applied to the brain. In the present study we sought to establish whether CNP was involved in the peripheral regulation of pancreatic 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, perivagal application of capsaicin and hexamethonium reduced CNP-evoked pancreatic flow and abolished chloride excretion but did not affect protein output. Furthermore, pre-treatment with atropine reduced both CNP-stimulated pancreatic flow and chloride excretion but failed to modify protein excretion. Partial muscarinic blockade of CNP-evoked chloride output suggested that mediators other 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 the activation of the 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. Present results suggest that CNP may play a role as a local regulator of the exocrine pancreas.

AB - We previously reported that C-type natriuretic peptide (CNP) increases amylase release in isolated pancreatic acini through natriuretic peptide receptor C activation and enhances pancreatic exocrine secretion via vagal pathways when applied to the brain. In the present study we sought to establish whether CNP was involved in the peripheral regulation of pancreatic 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, perivagal application of capsaicin and hexamethonium reduced CNP-evoked pancreatic flow and abolished chloride excretion but did not affect protein output. Furthermore, pre-treatment with atropine reduced both CNP-stimulated pancreatic flow and chloride excretion but failed to modify protein excretion. Partial muscarinic blockade of CNP-evoked chloride output suggested that mediators other 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 the activation of the 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. Present results suggest that CNP may play a role as a local regulator of the exocrine pancreas.

KW - Natriuretic peptide

KW - Natriuretic peptide receptor C

KW - Pancreatic exocrine secretion

KW - Vago-vagal reflex

UR - http://www.scopus.com/inward/record.url?scp=35448989408&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=35448989408&partnerID=8YFLogxK

U2 - 10.1016/j.ejphar.2007.08.043

DO - 10.1016/j.ejphar.2007.08.043

M3 - Article

C2 - 17900562

AN - SCOPUS:35448989408

VL - 577

SP - 192

EP - 202

JO - European Journal of Pharmacology

JF - European Journal of Pharmacology

SN - 0014-2999

IS - 1-3

ER -