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Regulation of intestinal secretion involved in the interaction between neurotransmitters and prostaglandin E 2
Author(s) -
Karaki S.I.,
Kuwahara A.
Publication year - 2004
Publication title -
neurogastroenterology and motility
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.489
H-Index - 105
eISSN - 1365-2982
pISSN - 1350-1925
DOI - 10.1111/j.1743-3150.2004.00482.x
Subject(s) - secretion , vasoactive intestinal peptide , acetylcholine , second messenger system , endocrinology , medicine , prostaglandin e2 , neurotransmitter , intracellular , cyclic adenosine monophosphate , extracellular , chemistry , biology , microbiology and biotechnology , neuropeptide , receptor , central nervous system
In this short review, it will be described that neurotransmitter‐induced secretion in the intestine may be influenced by the tissue level of prostaglandin E 2 (PGE 2 ). In the normal condition, vasoactive intestinal polypeptide (VIP) and acetylcholine (ACh) are the predominant neurotransmitters of secretomotor neurones. VIP and ACh activate distinct second messenger systems in epithelial cells, i.e. adenosine 3′, 5′‐cyclic monophosphate (cAMP) and calcium ion (Ca 2+ ), respectively. An increase in intracellular cAMP induces a small amount of chloride (Cl – ) secretion in epithelial cells, while simultaneous increases in intracellular Ca 2+ and cAMP greatly enhances the cAMP‐induced Cl – secretion. When the concentration of prostaglandins reaches a high level in the intestinal tissue substance P, which is a neurotransmitter of sensory neurones, can also induce a massive Cl – secretion by cross‐potentiation of cAMP and Ca 2+ in epithelial cells. In conclusion, it is considered that the concentration of tissue PGE 2 may indicate tissue alert level, and when this level elevates, PGE 2 enhances ACh and SP‐induced Cl – secretion, thus mediating massive fluid secretion for host defence.