title: Bile secretion is centrally regulated by C-type natriuretic peptide.
abstract: 1. Current evidence supports that C-type natriuretic peptide (CNP) is the brain natriuretic peptide. Natriuretic peptide receptors and mRNA CNP have been reported in the liver and in discrete areas and nucleus of the central nervous system involved in the regulation of gastrointestinal physiology. In the present work, we sought to establish the role of CNP in the central regulation of bile secretion in the rat and to delineate the possible pathways and mechanisms involved. 2. To examine the role of CNP on bile secretion, the peptide was applied in the brain lateral ventricle (1, 10, and 100 ng/microL) and bile samples were collected every 15 min for 60 min. The role of the autonomic nervous system in CNP response was assessed by atropine or combined phentolamine and propranolol administration. 3. Centrally applied CNP diminished basal as well as bile salt-evoked bile flow in a dose-dependent manner. CNP reduced bile acid output as well as sodium and potassium excretion, supporting CNP effect on bile acid-dependent flow. CNP also decreased chloride excretion and increased bile pH. The excretion of total glutathione was not affected by centrally applied CNP suggesting that this peptide does not alter bile acid-independent flow. Neither parasympathetic nor sympathetic blockade abolished CNP inhibitory response on bile secretion. Mean arterial pressure and portal venous pressure were not modified by CNP. 4. Present findings show that centrally applied CNP modulates bile secretion in a dose-dependent fashion. CNP alkalinized bile and reduced bile acid-dependent flow without affecting bile acid-independent flow. The inhibitory response of CNP on bile secretion was not mediated by the autonomic nervous system. Present findings give further support to the role of CNP as the brain natriuretic peptide.
authors.affiliation: Cátedras de Fisiopatología, Facultad de Farmacia y Bioquímica, Universidad de Buenos Aires, Buenos Aires, Argentina.
authors.forename: Maria E
authors.initials: ME
authors.lastname: Sabbatini
authors.forename: Marcelo S
authors.initials: MS
authors.lastname: Vatta
authors.forename: Cristina
authors.initials: C
authors.lastname: Vescina
authors.forename: José L
authors.initials: JL
authors.lastname: Castro
authors.forename: Belisario E
authors.initials: BE
authors.lastname: Fernández
authors.forename: Liliana G
authors.initials: LG
authors.lastname: Bianciotti
mesh_terms: D000818:Animals; D001341:Autonomic Nervous System / Q000187:drug effects / Q000502:physiology; D001646:Bile / Q000378:metabolism*; D001647:Bile Acids and Salts / Q000378:metabolism / Q000494:pharmacology; D001794:Blood Pressure / Q000187:drug effects / Q000502:physiology; D001921:Brain / Q000187:drug effects / Q000378:metabolism*; D004305:Dose-Response Relationship, Drug; D004573:Electrolytes / Q000378:metabolism; D006863:Hydrogen-Ion Concentration / Q000187:drug effects; D007276:Injections, Intraventricular; D008099:Liver / Q000378:metabolism*; D020098:Natriuretic Peptide, C-Type / Q000378:metabolism* / Q000494:pharmacology; D051381:Rats; D017207:Rats, Sprague-Dawley
chemical_list: D001647:Bile Acids and Salts; D004573:Electrolytes; D020098:Natriuretic Peptide, C-Type