title: Expression of NK-1 and NK-3 tachykinin receptors in pancreatic acinar cells after acute experimental pancreatitis in rats.
abstract: Activation of neurokinin (NK)-1 receptors but not of NK-3 stimulates amylase release from isolated pancreatic acini of the rat. Immunofluorescence studies show that NK-1 receptors are more strongly expressed than NK-3 receptors on pancreatic acinar cells under basal conditions. No studies have examined the expression of the two NK receptor populations in pancreatic acini during pancreatitis in rats. We therefore investigated the relationships between expression of these two tachykinin receptors and experimental acute pancreatitis induced by stimulating pancreatic amylase with caerulein (CK) in rats. Hyperstimulation of the pancreas by CK caused an increase in plasma amylase and pancreatic water content and resulted in morphological evidence of cytoplasmic vacuolization. Immunofluorescence analysis revealed a similar percentage of NK-1 receptor antibody immunoreactive acinar cells in rats with pancreatitis and in normal rat tissue but a larger percentage of NK-3 receptor immunoreactive cells in acute pancreatitis than in normal pancreas. Western blot analysis of NK-1 and NK-3 receptor protein levels after CK-induced pancreatitis showed no change in NK-1 receptors but a stronger increase in NK-3 receptor expression in pancreatic acini compared with normal rats thus confirming the immunofluorescence data. These new findings support previous evidence that substance P-mediated functions within the pancreas go beyond sensory signal transduction contributing to neurogenic inflammation, and they suggest that substance P plays a role in regulating pancreatic exocrine secretion via acinar NK-1 receptors. The significant increase in NK-3 receptors during pancreatic stimulation suggests that NK-3 receptors also intervene in the pathogenesis of mild acute pancreatitis in rats.
authors.affiliation: Dipartimento di Fisiologia Umana e Farmacologia "V. Erspamer" Università di Roma "La Sapienza"- P.le A. Moro 5-00185 Roma, Italia.
authors.forename: Maria
authors.initials: M
authors.lastname: Broccardo
authors.forename: Giorgio
authors.initials: G
authors.lastname: Linari
authors.forename: Simona
authors.initials: S
authors.lastname: Agostini
authors.forename: Giusi
authors.initials: G
authors.lastname: Amadoro
authors.forename: Francesco
authors.initials: F
authors.lastname: Carpino
authors.forename: Maria Teresa
authors.initials: MT
authors.lastname: Ciotti
authors.forename: Carla
authors.initials: C
authors.lastname: Petrella
authors.forename: Vincenzo
authors.initials: V
authors.lastname: Petrozza
authors.forename: Cinzia
authors.initials: C
authors.lastname: Severini
authors.forename: Giovanna
authors.initials: G
authors.lastname: Improta
mesh_terms: D000818:Animals; D002478:Cells, Cultured; D002108:Ceruletide; D004195:Disease Models, Animal; D015870:Gene Expression / Q000187:drug effects; D008297:Male; D010179:Pancreas / Q000187:drug effects / Q000378:metabolism* / Q000473:pathology*; D019283:Pancreatitis, Acute Necrotizing / Q000139:chemically induced / Q000378:metabolism* / Q000473:pathology*; D051381:Rats; D018040:Receptors, Neurokinin-1 / Q000378:metabolism*; D018042:Receptors, Neurokinin-3 / Q000378:metabolism*
chemical_list: D018040:Receptors, Neurokinin-1; D018042:Receptors, Neurokinin-3; D002108:Ceruletide