C-type natriuretic peptide enhances amylase release through NPR-C receptors in the exocrine pancreas
- Autores
- Sabbatini, María E.; Rodriguez, Myrian Roxana; Di Carlo, Maria Beatriz; Davio, Carlos Alberto; Vatta, Marcelo Sergio; Bianciotti, Liliana Graciela
- Año de publicación
- 2007
- Idioma
- inglés
- Tipo de recurso
- artículo
- Estado
- versión publicada
- Descripción
- Several studies show that C-type natriuretic peptide (CNP) has a modulatory role in the digestive system. CNP administration reduces both jejunal fluid and bile secretion in the rat. In the present study we evaluated the effect of CNP on amylase release in isolated pancreatic acini as well as the receptors and intracellular pathways involved. Results showed that all natriuretic peptide receptors were expressed not only in the whole pancreas but also in isolated pancreatic acini. CNP stimulated amylase secretion with a concentration-dependent biphasic response; maximum release was observed at 1 pM CNP, whereas higher concentrations gradually attenuated it. The response was mimicked by a selective natriuretic peptide receptor (NPR-C) agonist and inhibited by pertussis toxin, strongly supporting NPR-C receptor activation. CNP-evoked amylase release was abolished by U-73122 (PLC inhibitor) and 2-aminoethoxydiphenyl borate (2-APB) [an inositol 1,4,5-triphosphate (IP3) receptor antagonist], partially inhibited by GF-109203X (PKC inhibitor), and unaltered by ryanodine or protein kinase A (PKA) and protein kinase G (PKG) inhibitors. Phosphoinositide hydrolysis was enhanced by CNP at all concentrations and abolished by U-73122. At 1 and 10 pM, CNP did not affect cAMP or guanosine 3′,5′-cyclic monophosphate (cGMP) levels, but at higher concentrations it increased cGMP and diminished cAMP content. Present findings show that CNP stimulated amylase release through the activation of NPR-C receptors coupled to the PLC pathway and downstream effectors involved in exocytosis. The attenuation of amylase release was likely related to cAMP reduction. The augmentation in cGMP supports activation of NPR-A/NPR-B receptors probably involved in calcium influx. Present findings give evidence that CNP is a potential direct regulator of pancreatic function.
Fil: Sabbatini, María E.. No especifíca;
Fil: Rodriguez, Myrian Roxana. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina
Fil: Di Carlo, Maria Beatriz. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Departamento de Bioquímica Clínica; Argentina
Fil: Davio, Carlos Alberto. Universidad de Buenos Aires. Facultad de Ingeniería. Departamento de Física. Laboratorio de Radioisótopos; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay; Argentina
Fil: Vatta, Marcelo Sergio. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Química y Metabolismo del Fármaco. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Instituto de Química y Metabolismo del Fármaco; Argentina
Fil: Bianciotti, Liliana Graciela. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Departamento de Ciencias Biológicas. Cátedra de Fisiopatología; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay; Argentina - Materia
-
AMYLASE SECRETION
NATRIURETIC PEPTIDE RECEPTORS
PHOSPHOLIPASE C
PROTEIN KINASE C - Nivel de accesibilidad
- acceso abierto
- Condiciones de uso
- https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
- Repositorio
- Institución
- Consejo Nacional de Investigaciones Científicas y Técnicas
- OAI Identificador
- oai:ri.conicet.gov.ar:11336/241939
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CONICET Digital (CONICET) |
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C-type natriuretic peptide enhances amylase release through NPR-C receptors in the exocrine pancreasSabbatini, María E.Rodriguez, Myrian RoxanaDi Carlo, Maria BeatrizDavio, Carlos AlbertoVatta, Marcelo SergioBianciotti, Liliana GracielaAMYLASE SECRETIONNATRIURETIC PEPTIDE RECEPTORSPHOSPHOLIPASE CPROTEIN KINASE Chttps://purl.org/becyt/ford/3.1https://purl.org/becyt/ford/3Several studies show that C-type natriuretic peptide (CNP) has a modulatory role in the digestive system. CNP administration reduces both jejunal fluid and bile secretion in the rat. In the present study we evaluated the effect of CNP on amylase release in isolated pancreatic acini as well as the receptors and intracellular pathways involved. Results showed that all natriuretic peptide receptors were expressed not only in the whole pancreas but also in isolated pancreatic acini. CNP stimulated amylase secretion with a concentration-dependent biphasic response; maximum release was observed at 1 pM CNP, whereas higher concentrations gradually attenuated it. The response was mimicked by a selective natriuretic peptide receptor (NPR-C) agonist and inhibited by pertussis toxin, strongly supporting NPR-C receptor activation. CNP-evoked amylase release was abolished by U-73122 (PLC inhibitor) and 2-aminoethoxydiphenyl borate (2-APB) [an inositol 1,4,5-triphosphate (IP3) receptor antagonist], partially inhibited by GF-109203X (PKC inhibitor), and unaltered by ryanodine or protein kinase A (PKA) and protein kinase G (PKG) inhibitors. Phosphoinositide hydrolysis was enhanced by CNP at all concentrations and abolished by U-73122. At 1 and 10 pM, CNP did not affect cAMP or guanosine 3′,5′-cyclic monophosphate (cGMP) levels, but at higher concentrations it increased cGMP and diminished cAMP content. Present findings show that CNP stimulated amylase release through the activation of NPR-C receptors coupled to the PLC pathway and downstream effectors involved in exocytosis. The attenuation of amylase release was likely related to cAMP reduction. The augmentation in cGMP supports activation of NPR-A/NPR-B receptors probably involved in calcium influx. Present findings give evidence that CNP is a potential direct regulator of pancreatic function.Fil: Sabbatini, María E.. No especifíca;Fil: Rodriguez, Myrian Roxana. Consejo Nacional de Investigaciones Científicas y Técnicas; ArgentinaFil: Di Carlo, Maria Beatriz. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Departamento de Bioquímica Clínica; ArgentinaFil: Davio, Carlos Alberto. Universidad de Buenos Aires. Facultad de Ingeniería. Departamento de Física. Laboratorio de Radioisótopos; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay; ArgentinaFil: Vatta, Marcelo Sergio. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Química y Metabolismo del Fármaco. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Instituto de Química y Metabolismo del Fármaco; ArgentinaFil: Bianciotti, Liliana Graciela. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Departamento de Ciencias Biológicas. Cátedra de Fisiopatología; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay; ArgentinaAmerican Physiological Society2007-12info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionhttp://purl.org/coar/resource_type/c_6501info:ar-repo/semantics/articuloapplication/pdfapplication/pdfapplication/pdfapplication/pdfapplication/pdfapplication/pdfapplication/pdfhttp://hdl.handle.net/11336/241939Sabbatini, María E.; Rodriguez, Myrian Roxana; Di Carlo, Maria Beatriz; Davio, Carlos Alberto; Vatta, Marcelo Sergio; et al.; C-type natriuretic peptide enhances amylase release through NPR-C receptors in the exocrine pancreas; American Physiological Society; American Journal of Physiology-gastrointestinal and Liver Physiology; 293; 5; 12-2007; G987-G9940193-1857CONICET DigitalCONICETenginfo:eu-repo/semantics/altIdentifier/url/https://journals.physiology.org/doi/full/10.1152/ajpgi.00268.2007info:eu-repo/semantics/altIdentifier/doi/10.1152/ajpgi.00268.2007info:eu-repo/semantics/openAccesshttps://creativecommons.org/licenses/by-nc-sa/2.5/ar/reponame:CONICET Digital (CONICET)instname:Consejo Nacional de Investigaciones Científicas y Técnicas2025-09-29T09:33:47Zoai:ri.conicet.gov.ar:11336/241939instacron:CONICETInstitucionalhttp://ri.conicet.gov.ar/Organismo científico-tecnológicoNo correspondehttp://ri.conicet.gov.ar/oai/requestdasensio@conicet.gov.ar; lcarlino@conicet.gov.arArgentinaNo correspondeNo correspondeNo correspondeopendoar:34982025-09-29 09:33:47.771CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicasfalse |
dc.title.none.fl_str_mv |
C-type natriuretic peptide enhances amylase release through NPR-C receptors in the exocrine pancreas |
title |
C-type natriuretic peptide enhances amylase release through NPR-C receptors in the exocrine pancreas |
spellingShingle |
C-type natriuretic peptide enhances amylase release through NPR-C receptors in the exocrine pancreas Sabbatini, María E. AMYLASE SECRETION NATRIURETIC PEPTIDE RECEPTORS PHOSPHOLIPASE C PROTEIN KINASE C |
title_short |
C-type natriuretic peptide enhances amylase release through NPR-C receptors in the exocrine pancreas |
title_full |
C-type natriuretic peptide enhances amylase release through NPR-C receptors in the exocrine pancreas |
title_fullStr |
C-type natriuretic peptide enhances amylase release through NPR-C receptors in the exocrine pancreas |
title_full_unstemmed |
C-type natriuretic peptide enhances amylase release through NPR-C receptors in the exocrine pancreas |
title_sort |
C-type natriuretic peptide enhances amylase release through NPR-C receptors in the exocrine pancreas |
dc.creator.none.fl_str_mv |
Sabbatini, María E. Rodriguez, Myrian Roxana Di Carlo, Maria Beatriz Davio, Carlos Alberto Vatta, Marcelo Sergio Bianciotti, Liliana Graciela |
author |
Sabbatini, María E. |
author_facet |
Sabbatini, María E. Rodriguez, Myrian Roxana Di Carlo, Maria Beatriz Davio, Carlos Alberto Vatta, Marcelo Sergio Bianciotti, Liliana Graciela |
author_role |
author |
author2 |
Rodriguez, Myrian Roxana Di Carlo, Maria Beatriz Davio, Carlos Alberto Vatta, Marcelo Sergio Bianciotti, Liliana Graciela |
author2_role |
author author author author author |
dc.subject.none.fl_str_mv |
AMYLASE SECRETION NATRIURETIC PEPTIDE RECEPTORS PHOSPHOLIPASE C PROTEIN KINASE C |
topic |
AMYLASE SECRETION NATRIURETIC PEPTIDE RECEPTORS PHOSPHOLIPASE C PROTEIN KINASE C |
purl_subject.fl_str_mv |
https://purl.org/becyt/ford/3.1 https://purl.org/becyt/ford/3 |
dc.description.none.fl_txt_mv |
Several studies show that C-type natriuretic peptide (CNP) has a modulatory role in the digestive system. CNP administration reduces both jejunal fluid and bile secretion in the rat. In the present study we evaluated the effect of CNP on amylase release in isolated pancreatic acini as well as the receptors and intracellular pathways involved. Results showed that all natriuretic peptide receptors were expressed not only in the whole pancreas but also in isolated pancreatic acini. CNP stimulated amylase secretion with a concentration-dependent biphasic response; maximum release was observed at 1 pM CNP, whereas higher concentrations gradually attenuated it. The response was mimicked by a selective natriuretic peptide receptor (NPR-C) agonist and inhibited by pertussis toxin, strongly supporting NPR-C receptor activation. CNP-evoked amylase release was abolished by U-73122 (PLC inhibitor) and 2-aminoethoxydiphenyl borate (2-APB) [an inositol 1,4,5-triphosphate (IP3) receptor antagonist], partially inhibited by GF-109203X (PKC inhibitor), and unaltered by ryanodine or protein kinase A (PKA) and protein kinase G (PKG) inhibitors. Phosphoinositide hydrolysis was enhanced by CNP at all concentrations and abolished by U-73122. At 1 and 10 pM, CNP did not affect cAMP or guanosine 3′,5′-cyclic monophosphate (cGMP) levels, but at higher concentrations it increased cGMP and diminished cAMP content. Present findings show that CNP stimulated amylase release through the activation of NPR-C receptors coupled to the PLC pathway and downstream effectors involved in exocytosis. The attenuation of amylase release was likely related to cAMP reduction. The augmentation in cGMP supports activation of NPR-A/NPR-B receptors probably involved in calcium influx. Present findings give evidence that CNP is a potential direct regulator of pancreatic function. Fil: Sabbatini, María E.. No especifíca; Fil: Rodriguez, Myrian Roxana. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina Fil: Di Carlo, Maria Beatriz. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Departamento de Bioquímica Clínica; Argentina Fil: Davio, Carlos Alberto. Universidad de Buenos Aires. Facultad de Ingeniería. Departamento de Física. Laboratorio de Radioisótopos; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay; Argentina Fil: Vatta, Marcelo Sergio. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Química y Metabolismo del Fármaco. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Instituto de Química y Metabolismo del Fármaco; Argentina Fil: Bianciotti, Liliana Graciela. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Departamento de Ciencias Biológicas. Cátedra de Fisiopatología; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay; Argentina |
description |
Several studies show that C-type natriuretic peptide (CNP) has a modulatory role in the digestive system. CNP administration reduces both jejunal fluid and bile secretion in the rat. In the present study we evaluated the effect of CNP on amylase release in isolated pancreatic acini as well as the receptors and intracellular pathways involved. Results showed that all natriuretic peptide receptors were expressed not only in the whole pancreas but also in isolated pancreatic acini. CNP stimulated amylase secretion with a concentration-dependent biphasic response; maximum release was observed at 1 pM CNP, whereas higher concentrations gradually attenuated it. The response was mimicked by a selective natriuretic peptide receptor (NPR-C) agonist and inhibited by pertussis toxin, strongly supporting NPR-C receptor activation. CNP-evoked amylase release was abolished by U-73122 (PLC inhibitor) and 2-aminoethoxydiphenyl borate (2-APB) [an inositol 1,4,5-triphosphate (IP3) receptor antagonist], partially inhibited by GF-109203X (PKC inhibitor), and unaltered by ryanodine or protein kinase A (PKA) and protein kinase G (PKG) inhibitors. Phosphoinositide hydrolysis was enhanced by CNP at all concentrations and abolished by U-73122. At 1 and 10 pM, CNP did not affect cAMP or guanosine 3′,5′-cyclic monophosphate (cGMP) levels, but at higher concentrations it increased cGMP and diminished cAMP content. Present findings show that CNP stimulated amylase release through the activation of NPR-C receptors coupled to the PLC pathway and downstream effectors involved in exocytosis. The attenuation of amylase release was likely related to cAMP reduction. The augmentation in cGMP supports activation of NPR-A/NPR-B receptors probably involved in calcium influx. Present findings give evidence that CNP is a potential direct regulator of pancreatic function. |
publishDate |
2007 |
dc.date.none.fl_str_mv |
2007-12 |
dc.type.none.fl_str_mv |
info:eu-repo/semantics/article info:eu-repo/semantics/publishedVersion http://purl.org/coar/resource_type/c_6501 info:ar-repo/semantics/articulo |
format |
article |
status_str |
publishedVersion |
dc.identifier.none.fl_str_mv |
http://hdl.handle.net/11336/241939 Sabbatini, María E.; Rodriguez, Myrian Roxana; Di Carlo, Maria Beatriz; Davio, Carlos Alberto; Vatta, Marcelo Sergio; et al.; C-type natriuretic peptide enhances amylase release through NPR-C receptors in the exocrine pancreas; American Physiological Society; American Journal of Physiology-gastrointestinal and Liver Physiology; 293; 5; 12-2007; G987-G994 0193-1857 CONICET Digital CONICET |
url |
http://hdl.handle.net/11336/241939 |
identifier_str_mv |
Sabbatini, María E.; Rodriguez, Myrian Roxana; Di Carlo, Maria Beatriz; Davio, Carlos Alberto; Vatta, Marcelo Sergio; et al.; C-type natriuretic peptide enhances amylase release through NPR-C receptors in the exocrine pancreas; American Physiological Society; American Journal of Physiology-gastrointestinal and Liver Physiology; 293; 5; 12-2007; G987-G994 0193-1857 CONICET Digital CONICET |
dc.language.none.fl_str_mv |
eng |
language |
eng |
dc.relation.none.fl_str_mv |
info:eu-repo/semantics/altIdentifier/url/https://journals.physiology.org/doi/full/10.1152/ajpgi.00268.2007 info:eu-repo/semantics/altIdentifier/doi/10.1152/ajpgi.00268.2007 |
dc.rights.none.fl_str_mv |
info:eu-repo/semantics/openAccess https://creativecommons.org/licenses/by-nc-sa/2.5/ar/ |
eu_rights_str_mv |
openAccess |
rights_invalid_str_mv |
https://creativecommons.org/licenses/by-nc-sa/2.5/ar/ |
dc.format.none.fl_str_mv |
application/pdf application/pdf application/pdf application/pdf application/pdf application/pdf application/pdf |
dc.publisher.none.fl_str_mv |
American Physiological Society |
publisher.none.fl_str_mv |
American Physiological Society |
dc.source.none.fl_str_mv |
reponame:CONICET Digital (CONICET) instname:Consejo Nacional de Investigaciones Científicas y Técnicas |
reponame_str |
CONICET Digital (CONICET) |
collection |
CONICET Digital (CONICET) |
instname_str |
Consejo Nacional de Investigaciones Científicas y Técnicas |
repository.name.fl_str_mv |
CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicas |
repository.mail.fl_str_mv |
dasensio@conicet.gov.ar; lcarlino@conicet.gov.ar |
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1844613041324294144 |
score |
13.070432 |