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
CONICET Digital (CONICET)
Institución
Consejo Nacional de Investigaciones Científicas y Técnicas
OAI Identificador
oai:ri.conicet.gov.ar:11336/241939
Acceder
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network_name_str CONICET Digital (CONICET)
spelling 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 Técnicas2025-10-15T14:21:56Zoai: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:34982025-10-15 14:21:57.089CONICET 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
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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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score 13.22299

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