Natriuretic peptides as regulatory mediators of secretory activity in the digestive system.
Atrial natriuretic peptide (ANP) and C-type natriuretic peptide (CNP) are members of the natriuretic peptide family best known for their role in blood pressure regulation. However, in recent years all the natriuretic peptides and their receptors have been described in the gastrointestinal tract, digestive glands and central nervous system, as well as implicated in the regulation of digestive gland functions. The current review highlights the regulatory role of ANP and CNP in pancreatic and other digestive secretions. ANP and CNP stimulate basal as well as induced pancreatic secretion and modify bicarbonate and chloride secretions. Whereas ANP and CNP exert effects directly on pancreatic cells, CNP also acts through a vago-vagal reflex. At high doses both peptides attenuate pancreatic secretion induced by high doses of secretin through the PLC/PKC pathway. With regards to other digestive secretions, ANP and CNP decrease bile secretion in the rat. ANP does not induce salivation by itself but enhances stimulated salivary secretion and modifies salivary composition in rat parotid as well as submandibular glands. In rat pancreatic, hepatic, parotid and submandibular tissues, the NPR-C receptor mediates mostly peripheral responses whereas NPR-A and NPR-B receptors, which are coupled to guanylate cyclase, likely mediate the central response. In addition, ANP modulates gastric acid secretion via a vagal-dependent mechanism. In the intestine, ANP and CNP decrease water and sodium chloride absorption through an increase in cGMP levels. Overall, these findings indicate that ANP and CNP are members of the large group of regulatory peptides affecting digestive secretions.
Sabbatini
Maria Eugenia
ME
Department of Molecular and Integrative Physiology, University of Michigan, Ann Arbor, MI 48109-5622, United States. mesabba@umich.edu
D000818:Animals; D009320:Atrial Natriuretic Factor / Q000378:metabolism / Q000494:pharmacology*; D001639:Bicarbonates / Q000378:metabolism; D001646:Bile / Q000378:metabolism; D002712:Chlorides / Q000378:metabolism; D004064:Digestive System / Q000378:metabolism*; D004305:Dose-Response Relationship, Drug; D005744:Gastric Acid / Q000378:metabolism; D006801:Humans; D007408:Intestinal Absorption / Q000187:drug effects; D008954:Models, Biological; D045283:Natriuretic Agents / Q000494:pharmacology*; D020098:Natriuretic Peptide, C-Type / Q000378:metabolism / Q000494:pharmacology*; D046790:Pancreas, Exocrine / Q000187:drug effects / Q000294:innervation / Q000378:metabolism; D017461:Receptors, Atrial Natriuretic Factor / Q000378:metabolism*; D014630:Vagus Nerve / Q000502:physiology
D001639:Bicarbonates; D002712:Chlorides; D045283:Natriuretic Agents; D020098:Natriuretic Peptide, C-Type; D009320:Atrial Natriuretic Factor; D017461:Receptors, Atrial Natriuretic Factor