The somatostatin receptor-adenylate cyclase system in rat pancreatic acinar membranes after temporary pancreaticobiliary duct ligation

Authors
Rodríguez Martín, EulaliaUniversity of Alcalá Author; Álvaro Alonso, Itziar; Bodega Magro, GuillermoUniversity of Alcalá Author; Arilla Ferreiro, EduardoUniversity of Alcalá Author
Identifiers
Permanent link (URI): http://hdl.handle.net/10017/2250
DOI: 10.1016/S0024-3205(97)00930-2
ISSN: 0024-3205
Publisher
Elsevier
Date
1997
Affiliation
Universidad de Alcalá. Departamento de Bioquímica y Biología Molecular
Funders
The authors thank Ms. Carol F. Warren and Jerry Keller from the Alcala University Institution of Education Sciences and Lilian Puebla from the Department of Biochemistry of Alcala University for their linguistic assistance, as well as Ms. Maria Baez for her excellent assistance with library research and Mr. Luis Monge for assistance in the preparation of the illustrations. The authors are also grateful to Sandoz Ltd. (Basel, Switzerland) for generous donation of SMS 201-995 and its analogue Tyr3-SMS. This study was supported by a Grant from the Direction General de Investigación Científica y Técnica (PM95-0041) and from the University of Alcala (001/96) of Spain.
Bibliographic citation
Life Sciences, 1997, v. 61, n. 23, p. 2255-2269
Keywords
Pancreatitis
Somatostatin receptors
Exocrine pancreas
CAMP
Gi proteins
Project
PM95-0041 (Ministerio de Educación y Cultura)
001/96 (Universidad de Alcalá)
Document type
info:eu-repo/semantics/article
Version
info:eu-repo/semantics/publishedVersion
Publisher's version
http://dx.doi.org/10.1016/S0024-3205(97)00930-2
Rights
(c) Elsevier, 1997
Access rights
info:eu-repo/semantics/openAccess
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Abstract
The mechanism whereby somatostatin (SS) produces beneficial effects in established pancreatitis induced by pancreaticobiliary duct ligation (PBDL) is still not clear. The aim of the work was to evaluate the possibility of a direct action of SS on pancreatic acinar cells from rats with acute pancreatitis. For this purpose, we studied the SS-receptor-adenylate cyclase system in pancreatic acinar membranes from both, control rats and rats with experimentally induced acute pancreatitis. On the other hand, it has been reported that cholecystokinin (CCK) diminishes the number of SS receptors in pancreatic acinar cells. Proglumide, a CCK receptor antagonist reduces the severity of acute pancreatitis in the rat. Therefore, we have also examined the effect of proglumide on the somatostatinergic system in controls and rats with acute pancreatitis. Fourteen hours after PBDL, the SS receptors, the capacity of the SS analogue SMS 201-995 to inhibit forskolin-stimulated adenylate cyclase activity and PTX-catalyzed [P-32] ADP-ribosylation of the alpha(1) subunits of Gi proteins could not be detected in pancreatic acinar membranes. One month after reopening the closed pancreaticobiliary duct (PBD), the pancreas showed regeneration of acinar cells, and the above-mentioned parameters were significantly lower than in the control group. Two months after reopening the closed PBD, all these parameters had returned to control values. The administration of proglumide (20 mg/kg i.p.), a cholecystokinin receptor antagonist, accelerated pancreatic regeneration and approached all these parameters to control values one month after reopening the closed PBD. The present study suggests that the beneficial effects of SS on established pancreatitis induced by PBDL may not be due to a direct action of the peptide on pancreatic acinar cells at least at 14 hours after PBDL. In addition, these findings suggest that in established pancreatitis the effect of proglumide on the SS receptor-adenylate cyclase system could be due to its action on pancreatic regeneration.
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