PMID: 11910991Mar 26, 2002Paper

Vasoactive intestinal peptide is involved in the inhibitory effect of interleukin-1 beta on the jejunal contractile response induced by acetylcholine

Gastroentérologie Clinique Et Biologique
A C AubéJ P Galmiche

Abstract

Although previous studies have shown that interleukin-1 beta (IL-1 beta) decreases acetylcholine (ACh)-induced intestinal contraction by an action on the enteric nervous system, the neuromediator(s) involved are still unknown. To determine the role of nitric oxide (NO), vasoactive intestinal peptide (VIP) and/or adenosine triphosphate (ATP) in mediating this inhibitory effect. The effects of NO synthase inhibitors, VIP and ATP antagonists on motor response to the ACh were investigated before and after 90-min exposure of a rat preparation of jejunal longitudinal muscle-myenteric plexus to IL-1 beta. NG-nitro-L-arginine methyl ester, NG-nitro-L-arginine and NG-monomethyl-L-arginine were used to inhibit NO synthase, VIP (10-28) and [D-p-Cl-Phe6, Leu17] VIP to block VIP receptors, and suramin to block ATP receptors. NO synthase inhibitors failed to block the inhibitory effect of IL-1 beta on ACh-contracted jejunum smooth muscle. Suramin also failed to affect IL-1 beta-induced inhibition, whereas VIP antagonists abolished it. Moreover, the action of IL-1 beta was partly reproduced by VIP. While neither NO nor ATP accounts for the inhibitory effect of IL-1 beta on ACh-contracted jejunum, VIP seems to be a key-mediator of this effect.

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