Contribution of Nitric Oxide and Substance P to Nonadrenergic, Noncholinergic Transmission in the Guinea Pig Ileum

Changes of excitatory and inhibitory neurotransmitters in the colon of rats underwent to the wrap partial restraint stress

“…In rodents and humans, colonic nerve‐mediated relaxation is mainly purinergic and nitrergic and the loss of a small proportion of inhibitory neurons causes hypermotility . Moreover, in the rat colon, while functional experiments demonstrated that it is very difficult to obtain an SP mediated excitatory response, the pharmacological findings identified a complex neuronal circuit where SP, binding to neuronal NK1r, causes an increase in nitric oxide production that leads to muscle relaxation through the inhibition of cholinergic neurotransmission . To note, in the WRS rats the number of ChAT neurons are unchanged.…”

“…33,34 Moreover, in the rat colon, while functional experiments demonstrated that it is very difficult to obtain an SP mediated excitatory response, the pharmacological findings identified a complex neuronal circuit where SP, binding to neuronal NK1r, causes an increase in nitric oxide production that leads to muscle relaxation through the inhibition of cholinergic neurotransmission. 35,36 To note, in the WRS rats the number of ChAT neurons are unchanged. To summarize, in these animals, the probable functional impairment of the SP/NK1r and nNOS circuits releases the ChAT neurons from a negative control making them more active.…”

Chronic treatment with otilonium bromide induces changes in L‐type Ca2+channel, tachykinins, and nitric oxide synthase expression in rat colon muscle coat

“…9 Substance-P (SP) exerts an excitatory action directly on the SMC binding to the neurokinin receptor 1 (NK1r) and NK2r and an indirect inhibition of muscle contractility, binding to the NK1r located on the enteric neurons 10 through nitric oxide (NO) production. 11,12 Nitric oxide is produced by nitric oxide synthase (NOS) and, in the gut, two nNOS variants have been described, one expressed by a rich population of enteric neurons (nNOSb) and another located in the SMC (nNOSa). 13 Finally, it has been reported that OB behaves as an L-type Ca 2+ channel blocker 14 and this has been considered another action by which the drug reduces the exaggerated colonic motor activity present in IBS.…”

Control of non‐adrenergic non‐cholinergic reflex motor responses in circular muscle of guinea‐pig small intestine by Met‐enkephalin

“…Motor neurone which utilize mainly non‐adrenergic non‐cholinergic (NANC) transmitters, such as vasoactive intestinal peptide (VIP) and nitric oxide, underlie the descending motor response (Grider, 1993; waterman et al ., 1994). Nitric oxide is known as an inhibitory transmitter in the gut (Bult, Boecksxtaens, Pelckmans, Jordaes, Van Maercke & Herman, 1990), including the small intestine (Osthaus & Galligan, 1992; Williams & Parsons, 1995; Ivancheva, Itzev, Lolova & Radomirov, 1998) but both excitatory and inhibitory effects of nitric oxide on peristaltic activity of guinea‐pig small intestine were recently reported (Holzer, Lippe, Tabrizi, Lenard & Bartho, 1997). An interplay of somatostatin, GABA and opioid neurone was suggested to take part in the regulation of descending relaxation in circular muscle of the rat colon‐preparations (Grider, 1994).…”