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Receptor strategies in pancreatitis.

A variety of receptors on pancreatic acinar and duct cells regulate both pancreatic exocrine secretion and intracellular processes. These receptors are potential sites of action for therapeutic agents in the treatment of pancreatitis. Cholecystokinin (CCK) receptor antagonists, which may reduce the...

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Detalles Bibliográficos
Autor principal: Grendell, J. H.
Formato: Texto
Lenguaje:English
Publicado: Yale Journal of Biology and Medicine 1992
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2589733/
https://www.ncbi.nlm.nih.gov/pubmed/1340060
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author Grendell, J. H.
author_facet Grendell, J. H.
author_sort Grendell, J. H.
collection PubMed
description A variety of receptors on pancreatic acinar and duct cells regulate both pancreatic exocrine secretion and intracellular processes. These receptors are potential sites of action for therapeutic agents in the treatment of pancreatitis. Cholecystokinin (CCK) receptor antagonists, which may reduce the level of metabolic "stress" on acinar cells, have been shown to mitigate the severity of acute pancreatitis in a number of models. Not all studies have shown a benefit, however, and differences may exist between different structural classes of antagonists. Because increased pancreatic stimulation due to loss of feedback inhibition of CCK has been proposed to contribute to the pain of some patients with chronic pancreatitis, CCK receptor antagonists could also be of benefit in this setting. Somatostatin and its analogs diminish pancreatic secretion of water and electrolytes and have been effective in treating pancreatic fistulas and pseudocysts. These agents are also being evaluated for their ability to reduce pain in chronic pancreatitis (perhaps by reducing ductal pressure by diminishing secretory volume) and mitigating the severity of acute pancreatitis (possibly by reducing the metabolic load on acinar cells). Recently described secretin receptor antagonists may also have therapeutic value as a means of selectively inhibiting pancreatic secretion of water and electrolytes.
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spelling pubmed-25897332008-11-28 Receptor strategies in pancreatitis. Grendell, J. H. Yale J Biol Med Research Article A variety of receptors on pancreatic acinar and duct cells regulate both pancreatic exocrine secretion and intracellular processes. These receptors are potential sites of action for therapeutic agents in the treatment of pancreatitis. Cholecystokinin (CCK) receptor antagonists, which may reduce the level of metabolic "stress" on acinar cells, have been shown to mitigate the severity of acute pancreatitis in a number of models. Not all studies have shown a benefit, however, and differences may exist between different structural classes of antagonists. Because increased pancreatic stimulation due to loss of feedback inhibition of CCK has been proposed to contribute to the pain of some patients with chronic pancreatitis, CCK receptor antagonists could also be of benefit in this setting. Somatostatin and its analogs diminish pancreatic secretion of water and electrolytes and have been effective in treating pancreatic fistulas and pseudocysts. These agents are also being evaluated for their ability to reduce pain in chronic pancreatitis (perhaps by reducing ductal pressure by diminishing secretory volume) and mitigating the severity of acute pancreatitis (possibly by reducing the metabolic load on acinar cells). Recently described secretin receptor antagonists may also have therapeutic value as a means of selectively inhibiting pancreatic secretion of water and electrolytes. Yale Journal of Biology and Medicine 1992 /pmc/articles/PMC2589733/ /pubmed/1340060 Text en
spellingShingle Research Article
Grendell, J. H.
Receptor strategies in pancreatitis.
title Receptor strategies in pancreatitis.
title_full Receptor strategies in pancreatitis.
title_fullStr Receptor strategies in pancreatitis.
title_full_unstemmed Receptor strategies in pancreatitis.
title_short Receptor strategies in pancreatitis.
title_sort receptor strategies in pancreatitis.
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2589733/
https://www.ncbi.nlm.nih.gov/pubmed/1340060
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