Submitted on October 26, 2005
Accepted on April 18, 2006
EXPRESSION OF NK-1 AND NK-3 TACHYKININ RECEPTORS IN PANCREATIC ACINAR CELLS AFTER ACUTE EXPERIMENTAL PANCREATITIS IN RATS
Maria Broccardo1, Giorgio Linari1, Simona Agostini1, Giusi Amadoro2, Francesco Carpino3, Maria Teresa Ciotti2, Carla Petrella1, Vincenzo Petrozza3, Cinzia Severini2, and Giovanna Improta1*
1 Department of Human Physiology and Pharmacology, University of Rome "La Sapienza", Rome, Italy
2 Institute of Neurobiology and Molecular Medicine, CNR, Rome, Italy
3 Department Experimental medicine and Biopathology, University of Rome "La Sapienza", Rome, Italy
* To whom correspondence should be addressed. E-mail: giovanna.improta{at}uniroma1.it.
Activation of neurokinin-1 (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 TK 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 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 in comparison with normal rats thus confirming the immunofluorescence data. These new findings support previous evidence that SP-mediated functions within the pancreas go beyond sensory signal transduction contributing to neurogenic inflammation, and suggest that SP 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.
