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

Although previous studies have shown that interleukin-1ß (IL-1ß) decreases acetylcholine (ACh)-induced intestinal contraction by an action on the enteric nervous system, the neuromediator(s) involved are still unknow.

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-1ß. 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-Phe ⁶ , Leu ¹⁷ ] VIP to block VIP receptors, and suramin to block ATP receptors.

NO synthase inhibitors failed to block the inhibitory effect of IL-1ß on ACh-contracted jejunum smooth muscle. Suramin also failed to affect IL-1ß-induced inhibition, whereas VIP antagonists abolished it. Moreover, the action of IL-1ß was partly reproduced by VIP.

While neither NO nor ATP accounts for the inhibitory effect of IL-1ß on ACh-contracted jejunum, VIP seems to be a key-mediator of this effect.