Non-adrenergic non-cholinergic neuron stimulation in the cat lower esophageal sphincter

Kortezova, N; Mizhorkova, Z.; Milusheva, E.; Varga, Gábor; Vizi, E.S.; Papasova, M

doi:10.1016/0014-2999(96)00093-3

Cited by 19 publications

(17 citation statements)

References 28 publications

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“…Many neurotransmitters including substance P and vasoactive intestinal peptide are proposed to be involved in the contractile response in the mouse distal colon (36 -38). Nicotine-induced relaxation seemed to be due to the release of vasoactive intestinal peptiderelated peptides in the guinea-pig caecum (39) and cat esophageal sphincter (40). In preliminary experiments, nicotine-induced relaxation appeared to be partially (approximately 30%) inhibited in the distal colon treated with 1 μM phentolamine.…”

Section: Conclusion and Future Problemsmentioning

confidence: 89%

Nicotine-Induced Neurogenic Relaxation in the Mouse Colon: Changes With Dextran Sodium Sulfate–Induced Colitis

et al. 2009

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Abstract. Nicotine has been shown to reduce both tone and muscular activity in the human colon by releasing nitric oxide (NO) from nerves. To our knowledge, however, the effect of nicotine on mouse colon has not been elucidated, and the response in tissue from ulcerative colitis (UC) has not been investigated. We examined nicotine-induced responses in colon from control mice and mice with dextran sodium sulfate (DSS)-induced UC. In controls, bath application of nicotine caused a transient relaxation in longitudinal preparations from the transverse and distal colons but not from the rectum. The response was observed in the presence of bethanechol, abolished by treatment with tetrodotoxin and hexamethonium, and mediated partially (>50%) by the NO pathway. In longitudinal preparations of the distal colon from DSStreated mice, spontaneous contractions decreased markedly, and nicotine caused contraction without relaxation in half of the preparations tested. Nicotine-induced relaxation in the presence of bethanechol was significantly decreased in the DSS-treated distal colon without changing bethanechol-induced contractions. These data suggest that 1) responses to nicotine differ dependent on colon regions, 2) DSS treatment predominantly caused nicotine-sensitive neurogenic changes in distal colon, and 3) DSS treatment may reverse the direction of nicotine-evoked responses in the colon, in mice.

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Section: Conclusion and Future Problemsmentioning

confidence: 89%

Nicotine-Induced Neurogenic Relaxation in the Mouse Colon: Changes With Dextran Sodium Sulfate–Induced Colitis

et al. 2009

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“…The nonadrenergic, noncholinergic neurotransmitters NO, VIP, PACAP, ATP, calcitonin gene-related polypeptide (CGRP), and CO all have inhibitory effects in the gastrointestinal tract. Immunohistochemistry of the LES myenteric neurons shows the presence of NOS, the peptides VIP, PACAP, and CGRP, and the constitutive enzyme heme oxygenase type 2 that is involved in the synthesis of CO (De Man et al, 1991;Murray et al, 1991;Tłottrup et al, 1991;Oliveira et al, 1992;Tøttrup et al, 1993;Kortezova et al, 1996;Yuan et al, 1998;Farre et al, 2006;Farré et al, 2007).…”

Section: Discussionmentioning

confidence: 99%

Pharmacologic Specificity of Nicotinic Receptor-Mediated Relaxation of Muscarinic Receptor Precontracted Human Gastric Clasp and Sling Muscle Fibers within the Gastroesophageal Junction

Braverman

Vegesna²,

Miller³

et al. 2011

The Journal of Pharmacology and Experimental Therapeutics

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Relaxation of gastric clasp and sling muscle fibers is involved the transient lower esophageal sphincter relaxations underlying the pathophysiology of gastroesophageal reflux disease (GERD). These fibers do not contribute tone to the high-pressure zone in GERD patients, indicating their role in pathophysiology. This study identifies some mediators of the nicotine-induced relaxation of muscarinic receptor precontracted gastric clasp and sling fibers. Muscle strips from organ donors precontracted with bethanechol were relaxed with nicotine and then rechallenged after washing and adding inhibitors tetrodotoxin (TTX), the nitric-oxide synthase inhibitor L-nitro-arginine methyl ester (L-NAME), the ␤-adrenoceptor antagonist propranolol, the glycine receptor antagonist strychnine or ginkgolide B, and the GABA A receptor antagonist bicuculline or 2-(3-carboxypropyl)-3-amino-6-(4 methoxyphenyl)pyridazinium bromide [(gabazine) SR95531]. TTX only inhibited clasp fiber relaxations. L-NAME and propranolol inhibited, and ginkgolide B was ineffective in both. SR95531 was ineffective in clasp fibers and partially effective in sling fibers. Strychnine and bicuculline prevented relaxations with low potency, indicating actions not on glycine or GABA A receptors but more consistent with nicotinic receptor blockade. Bethanechol-precontracted fibers were relaxed by the nitric oxide donor S-nitroso-N-acetyl-DL-penicillamine and by the ␤-adrenergic agonist isoproterenol (clasp fibers only) but not by the glycine receptor agonist taurine or glycine or the GABA A agonist muscimol. These data indicate that nicotinic receptor activation mediates relaxation via release of nitric oxide in clasp and sling fibers, norepinephrine acting on ␤-adrenoceptors in clasp fibers, and GABA acting on GABA A receptors in sling fibers. Agents that selectively prevent these relaxations may be useful in the treatment of GERD.

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“…It has been reported that NANC inhibitory responses are mainly mediated by nitrergic nerves in esophagus from the opossum (Christinck et al, 1991;Murray et al, 1991), cat (Ny et al, 1995), cow (Barahona et al, 1998), and human (Richards et al, 1995) and also in the LES from the dog Daniel et al, 2002), opossum (Tottrup et al, 1991a,b;Conklin et al, 1993;Uc et al, 1999), guinea pig (Imaeda et al, 1998), cat (Kortezova et al, 1996), mouse (Kim et al, 1999;Sivarao et al, 2001), and human (McKirdy et al, 1992;Preiksaitis et al, 1994;Tomita et al, 1997). Biphasic, rapid and sustained, relaxations of the feline LES are suggested to be mediated by NO and VIP or VIP-like peptides (Kortezova et al, 1996), and those of the opossum sphincter appear to be mediated by NO and an unidentified substance (Uc et al, 1999).…”

Section: A Esophagusmentioning

confidence: 99%

“…Biphasic, rapid and sustained, relaxations of the feline LES are suggested to be mediated by NO and VIP or VIP-like peptides (Kortezova et al, 1996), and those of the opossum sphincter appear to be mediated by NO and an unidentified substance (Uc et al, 1999). In LES strips from humans, inhibitory motorneurons were efficiently stimulated both by electrical field stimulation and stimulation of nicotinic receptors located in nerve terminals, releasing NO and an apamin-sensitive neurotransmitter (Gonzalez et al, 2004).…”

Section: A Esophagusmentioning

confidence: 99%

Gastrointestinal Function Regulation by Nitrergic Efferent Nerves

Toda

Herman

2005

Pharmacological Reviews

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Non-adrenergic non-cholinergic neuron stimulation in the cat lower esophageal sphincter

Cited by 19 publications

References 28 publications

Nicotine-Induced Neurogenic Relaxation in the Mouse Colon: Changes With Dextran Sodium Sulfate–Induced Colitis

Nicotine-Induced Neurogenic Relaxation in the Mouse Colon: Changes With Dextran Sodium Sulfate–Induced Colitis

Pharmacologic Specificity of Nicotinic Receptor-Mediated Relaxation of Muscarinic Receptor Precontracted Human Gastric Clasp and Sling Muscle Fibers within the Gastroesophageal Junction

Gastrointestinal Function Regulation by Nitrergic Efferent Nerves

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