Interplay between nitric oxide and vasoactive intestinal polypeptide in the pig gastric fundus smooth muscle

Dick, J M C; Lefebvre, Romain

doi:10.1016/s0014-2999(00)00299-5

Cited by 11 publications

(10 citation statements)

References 39 publications

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“…In addition to NO, other transmitters such as VIP or ATP are implicated in NANC relaxations of the rat gastric fundus (7,47,48). The present results do not support a role for VIP or ATP in the hypo-contractility induced by endotoxin.…”

Section: Sgc and Small Conductance Ca K + Channels Mediate Fundus Hypcontrasting

confidence: 83%

Synthesis of nitric oxide in post‐ganglionic myenteric neurons during endotoxemia: implications for gastric motor function

Quintana¹,

Hernández

Álvarez-Barrientos

et al. 2004

FASEB j.

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We have investigated the mechanisms underlying acute changes in gastric motor function triggered by endotoxemia. In fundal strips from rats pre-treated with endotoxin (40 microg/kg, i.p. 30 min), mechanical activity was analyzed and the source of nitric oxide (NO) was visualized by confocal microscopy of tissue loaded with the fluorescent dye DAF-FM. NOS expression was determined by quantitative RT-PCR and Western blot, and enzyme activity by the citrulline assay. Strips from endotoxin-treated rats were hypo-contractile. This was prevented by pre-incubation with the neurotoxin tetrodotoxin, the gangliar blocker hexamethonium, or non-selective and neuronal-specific NOS inhibitors (L-NOARG and TRIM, respectively). The soluble guanylyl cyclase (sGC) inhibitor ODQ and the inhibitor of small conductance Ca2+-activated K+ channels apamin prevented relaxation induced by endotoxin, nicotine, exogenous NO (DETA-NONOate), and the NO-independent sGC activator BAY 41-2272. NO synthesis was observed in neuronal soma, axons, and nerve endings of the myenteric plexus in the fundus of endotoxin-treated rats and was prevented by L-NAME, tetrodotoxin, and hexamethonium. nNOS and iNOS mRNA and protein contents were unchanged. Our findings demonstrate synthesis of NO in post-ganglionic myenteric neurons during early endotoxemia that mediates gastric hypo-contractility. The effect of NO is mediated via sGC and small conductance Ca2+-activated K+channels.

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Section: Sgc and Small Conductance Ca K + Channels Mediate Fundus Hypcontrasting

confidence: 83%

Synthesis of nitric oxide in post‐ganglionic myenteric neurons during endotoxemia: implications for gastric motor function

Quintana¹,

Hernández

Álvarez-Barrientos

et al. 2004

FASEB j.

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“…Jin et al (1996) and Murthy et al (1996) suggested the dual origin of NO from nerves and muscle and its interplay with VIP in regulating relaxation of the rabbit and rat stomach. Recent studies by Dick and Lefebvre (2000) and Dick et al (2001Dick et al ( , 2002 on pig, guinea pig, and mouse gastric fundus smooth muscle cells have provided evidence that inducible NOS probably induced by the isolation procedure may be involved in the relaxant effect of VIP, thereby underscoring the importance of the experimental method used. From findings that nicotine-induced NANC relaxation in the gastric fundus was reduced by a specific anti-VIP serum and that nicotine increased the outflow of VIP-and histidine isoleucine-like immunoreactivity from the strips, involvement of VIP and possibly histidine isoleucine in the mechanical response was suggested (Curro and Preziosi, 1997).…”

Section: Cotransmitters Responsible For Nonadrenergic Noncholinergmentioning

confidence: 99%

Gastrointestinal Function Regulation by Nitrergic Efferent Nerves

Toda

Herman

2005

Pharmacol Rev

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“…Furthermore, relaxation by VIP is produced partially via activation of adenylate cyclase and partially via stimulation of NO production in the smooth muscle. Said NO may relax the smooth muscle through activation of sGC and diffuse back to the nerve terminal to further enhance VIP release (Dick & Lefebvre, 2000; Teng et al ., 1988).…”

Section: Introductionmentioning

confidence: 99%