| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH |
|
|
|
|||||||
|
|||||||||
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
1 Catedra de Fisiopatologia, Universidad de Buenos Aires, Facultad de Farmacia y Bioquimica, Buenos Aires, Bs As, Argentina
2 Departamento de Analisis Clinicos, Universidad de Buenos Aires, Facultad de Farmacia y Bioquimica, Buenos Aires, Bs As, Argentina
3 Laboratorio de Radioisotopos, Universidad de Buenos Aires-FFyB, Buenos Aires, Bs As, Argentina
4 Catedra de Fisiologia (IQUIMEFA-CONICET), Universidad de Buenos Aires, Facultad de Farmacia y Bioquimica, Buenos Aires, Bs As, Argentina
* To whom correspondence should be addressed. E-mail: lbianc{at}ffyb.uba.ar.
Increasing evidence supports the role of atrial natriuretic factor (ANF) in the modulation of gastrointestinal physiology. The effect of ANF on exocrine pancreatic secretion and the possible receptors and pathways involved were studied in vivo. Anesthetized rats were prepared with pancreatic duct cannulation, pyloric ligation, and bile diversion into the duodenum. ANF dose-dependently increased pancreatic secretion of fluid and proteins and enhanced secretin and CCK-evoked response. ANF decreased chloride secretion and increased the pH of the pancreatic juice. Neither cholinergic nor adrenergic blockade affected ANF-stimulated pancreatic secretion. Further ANF response was not mediated by the release of nitric oxide (NO). ANF-evoked protein secretion was not inhibited by truncal vagotomy, atropine or L-NAME administration. The selective NPR-C receptor agonist, cANP (4-23), mimicked ANF response in a dose dependent fashion. When the intracellular signaling coupled to NPR-C receptors was investigated in isolated pancreatic acini results showed that ANF did not modify basal or forskolin-evoked cAMP formation but it dose-dependently enhanced phosphoinositide hydrolysis that was blocked by the selective PLC inhibitor U-73122. ANF stimulated exocrine pancreatic secretion in the rat and its effect was not mediated by NO, parasympathetic or sympathetic activity. Further, CCK and secretin appear not to be involved in ANF response. Present findings support that ANF exerts a stimulatory effect on pancreatic exocrine secretion mediated by NPR-C receptors coupled to the phosphoinositide pathway.
This article has been cited by other articles:
|
|
 |
|
  M. E. Sabbatini, X. Chen, S. A. Ernst, and J. A. Williams Rap1 Activation Plays a Regulatory Role in Pancreatic Amylase Secretion J. Biol. Chem., August 29, 2008; 283(35): 23884 - 23894. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 M. William, E. J. Hamilton, A. Garcia, H. Bundgaard, K. K. M. Chia, G. A. Figtree, and H. H. Rasmussen Natriuretic peptides stimulate the cardiac sodium pump via NPR-C-coupled NOS activation Am J Physiol Cell Physiol, April 1, 2008; 294(4): C1067 - C1073. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 M. E. Sabbatini, M. Rodriguez, M. B. di Carlo, C. A. Davio, M. S. Vatta, and L. G. Bianciotti C-type natriuretic peptide enhances amylase release through NPR-C receptors in the exocrine pancreas Am J Physiol Gastrointest Liver Physiol, November 1, 2007; 293(5): G987 - G994. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
M. E. Sabbatini, M. S. Vatta, C. A. Davio, and L. G. Bianciotti Atrial natriuretic factor negatively modulates secretin intracellular signaling in the exocrine pancreas Am J Physiol Gastrointest Liver Physiol, January 1, 2007; 292(1): G349 - G357. [Abstract] [Full Text] [PDF]
|
|
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH |
| Visit Other APS Journals Online |
