Role of nitric oxide in norepinephrine release from myenteric plexus in vitro and in Trichinella spiralis-infected rats.

Abstract

Nitric oxide (NO) has been implicated as modulator of neural function and inflammatory mediator. Previously, we have demonstrated suppression of norepinephrine (NE) release from myenteric nerves following Trichinella spiralis infection implicating interleukin-1 beta (IL-1 beta) as a mediator of these changes. In the present study, we have examined the role of NO in NE release from the myenteric plexus and in the suppression of NE release induced by IL-1 beta in vitro, and we have determined whether NO is involved in the suppression of NE release from the myenteric plexus observed in T. spiralis-infected rats. Electrically evoked NE release from jejunal longitudinal muscle-myenteric plexus preparations (LMMP) was measured following (a) in vitro exposure of the tissue to the NO donor 3-morpholinosydnonimine (SIN-1), L-arginine, or IL-1 beta, in the presence or absence of NOS inhibitors, and (b) in vivo treatment of control or T. spiralis-infected rats with N6-nitro-L-arginine-methyl-ester (L-NAME), NG-nitro-D-arginine-methyl-ester (D-NAME) or vehicle for 6 days. In vitro inhibition of NO synthesis had no effect on NE release from the myenteric plexus. Treatment with SIN-1 or L-arginine suppressed NE release in a manner similar to that observed with IL-1 beta. Moreover, the effect of IL-1 beta was attenuated by L-NAME. In contrast, treatment of T. spiralis-infected rats with L-NAME had no effect on the suppression of NE release. These results indicate that in the absence of inflammation, the myenteric plexus can generate sufficient NO to inhibit NE release and that NO mediates the action of IL-1 beta on NE release in vitro. However, we have no evidence for the involvement of NO in the suppression of NE release in nematode-infected rats.