Evidence that nitric oxide acts as an inhibitory neurotransmitter supplying taenia from the guinea‐pig caecum

Shuttleworth, C. William; Sweeney, Kathy; Sanders, Kenton M.

doi:10.1038/sj.bjp.0702674

Cited by 24 publications

(22 citation statements)

References 31 publications

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“…NO contributes directly to a component of inhibitory transmission in guinea-pig T. coli [136], therefore a possible role of L-arginine-NO pathway is presented in the modulation of transmission in this guineapig cestoda [137]. In addition, the source and role of basal NO in vitro in proximal segments of another species of taenia (T. caeci) in guinea pig was also indicated [138].…”

Section: Taenia Spmentioning

confidence: 99%

Involvement of nitric oxide and its up/down stream molecules in the immunity against parasitic infections

Nahrevanian

2009

Braz J Infect Dis

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Nitric oxide (NO) is a potent mediator with diverse roles in regulating cellular functions and signaling pathways. The NO synthase (NOS) enzyme family consists of three major isoforms, which convey variety of messages between cells, including signals for vasorelaxation, neurotransmission and cytotoxicity. This family of enzymes are generally classified as neuronal NOS (nNOS), endothelial NOS (eNOS) and inducible NOS (iNOS). Increased levels of NO are induced from iNOS during infection; while eNOS and nNOS may be produced at the baseline in normal conditions. An association of some key cytokines appears to be essential for NOS gene regulation in the immunity of infections. Accumulating evidence indicates that parasitic diseases are commonly associated with elevated production of NO. NO plays a role in the immunoregulation and it is implicated in the host non-specific defence in a variety of infections. Nevertheless, the functional role of NO and NOS isoforms in the immune responses of host against the majority of parasites is still highly controversial. In the present review, the role of parasitic infections will be discussed in the controversy related to the NO production and iNOS gene expression in different parasites and a variety of experimental models.

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Section: Taenia Spmentioning

confidence: 99%

Involvement of nitric oxide and its up/down stream molecules in the immunity against parasitic infections

Nahrevanian

2009

Braz J Infect Dis

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“…gastrointestinal motility; adenosine 5Ј-triphosphate; voltagedependent nonselective cation current GASTROINTESTINAL (GI) motility is orchestrated by the enteric nervous system activating and inhibiting GI muscles in orderly patterns. The inhibitory component of neuromuscular regulation comes from release of several neurotransmitter substances, including ATP, NO, and peptides (4,10,21). In GI muscles such as human, murine, and guinea pig colon, release of ATP during nerve stimulation evokes a fast inhibitory junction potential (IJP), which transiently takes the membrane potentials of smooth muscle cells toward the equilibrium potential for the K ϩ ionic gradient (hyperpolarization) (8,22).…”

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confidence: 99%

Mechanism of active repolarization of inhibitory junction potential in murine colon

Baker

Mutafova‐Yambolieva

Monaghan

et al. 2003

American Journal of Physiology-Gastrointestinal and Liver Physi

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. Mechanism of active repolarization of inhibitory junction potential in murine colon. Am J Physiol Gastrointest Liver Physiol 285: G813-G821, 2003; 10.1152/ajpgi. 00115.2003.-Enteric inhibitory responses in gastrointestinal (GI) smooth muscles involve membrane hyperpolarization that transiently reduce the excitability of GI muscles. We examined the possibility that an active repolarization mechanism participates in the restoration of resting membrane potential after fast inhibitory junction potentials (IJPs) in the murine colon. Previously, we showed these cells express a voltage-dependent nonselective cation conductance (NSCC) that might participate in active repolarization of IJPs. Colonic smooth muscle cells were impaled with microelectrodes and voltage responses to nerve-evoked IJPs, and locally applied ATP were recorded. Ba 2ϩ (500 M), a blocker of the NSCC, slowed the rate of repolarization of IJPs. We also tested the effects of Ba 2ϩ , Ni 2ϩ , and mibefradil, all blockers of the NSCC, on responses to locally applied ATP. Spritzes of ATP caused transient hyperpolarization, and the durations of these responses were significantly increased by the blockers of the NSCC. We considered whether NSCC blockers might affect ATP metabolism and found that Ni 2ϩ decreased ATP breakdown in colonic muscles. Mibefradil had no effect on ATP metabolism. Because both Ni 2ϩ and mibefradil had similar effects on prolonging responses to ATP, it appears that restoration of resting membrane potential after ATP spritzes is not primarily due to ATP metabolism. Neurally released enteric inhibitory transmitter and locally applied ATP resulted in transient hyperpolarizations of murine colonic muscles. Recovery of membrane potential after these responses appears to involve an active repolarization mechanism due to activation of the voltage-dependent NSCC expressed by these cells. gastrointestinal motility; adenosine 5Ј-triphosphate; voltagedependent nonselective cation current GASTROINTESTINAL (GI) motility is orchestrated by the enteric nervous system activating and inhibiting GI muscles in orderly patterns. The inhibitory component of neuromuscular regulation comes from release of several neurotransmitter substances, including ATP, NO, and peptides (4, 10, 21). In GI muscles such as human, murine, and guinea pig colon, release of ATP during nerve stimulation evokes a fast inhibitory junction potential (IJP), which transiently takes the membrane potentials of smooth muscle cells toward the equilibrium potential for the K ϩ ionic gradient (hyperpolarization) (8,22). Release of NO during the same period results in a smaller amplitude and longer-duration hyperpolarization phase that can outlast the fast phase of the IJP by several times. The fast hyperpolarization arises from activation of apamin-sensitive, small-conductance Ca 2ϩ -activated K ϩ channels (SK) (14), and the slow phase of the IJP is due to NOdependent stimulation of cyclic GMP production, activation of protein kinase G, and activation of NO-dependent K conductance(s) (5,...

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“…The tension of the smooth muscle is mainly determined by the amount of phosphorylated myosin light chain (MLC), which is related to intracellular Ca 2+ concentration (14) and guinea pig caecum (19). Charybdotoxin, an inhibitor of large conductance Ca…”

Section: +mentioning

confidence: 99%

Mechanism of a Nitric Oxide Donor NOR 1-Induced Relaxation in Longitudinal Muscle of Rat Proximal Colon

Takeuchi

Sugimoto

Morimoto

et al. 2001

Japanese Journal of Pharmacology

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ABSTRACT-We previously suggested that nitric oxide (NO)-mediated relaxation of the rat proximal colon is not associated with change in cyclic GMP content. We further studied the intracellular mechanism of NOinduced relaxation by measuring changes in tension and intracellular Ca 2+ concentration ([Ca 2+ ]i), simultaneously. NOR 1, NO donor, relaxed the longitudinal muscle of the rat proximal colon, which was precontracted by carbachol, with a concomitant decrease in [Ca 2+ ]i. ODQ, an inhibitor of soluble guanylate cyclase, partially inhibited the relaxant effect of only higher concentrations of NOR 1, but Rp-8-Br-cGMPS, an inhibitor of cyclic GMP-dependent protein kinase (PKG), did not have any effects on the relaxant effect of NOR 1. When the preparations were transferred to normal solution after the treatment with thapsigargin, an inhibitor of sarcoplasmic reticulum (SR) Ca ]i, although a cyclic GMP-PKG pathway is suggested under the experimental conditions of a high K + concentration.Keywords: Nitric oxide-induced relaxation, NOR 1, Rat proximal colon, Decrease in intracellular Ca 2+ concentration, Sarcoplasmic reticulum Nitric oxide (NO) has been reported to mediate nonadrenergic, non-cholinergic (NANC) relaxation in various regions of the gastrointestinal tract (for reviews, see refs. 1 -3). However, the intracellular mechanism of relaxation induced by NO is not clarified yet.It was shown that an elevation in cyclic GMP content was associated with electrical field stimulation (EFS)-induced relaxation in the opossum (4) and human (5) lower esophageal sphincter and the canine internal anal sphincter (6). NO is known to increase the intracellular cyclic GMP content through an activation of soluble guanylate cyclase in vascular smooth muscles (7). It was also shown that NO or EFS which induces NO-mediated relaxation, increased the cyclic GMP content in the smooth muscle cells in the rat ileum (8) and proximal colon (9). These results suggest that NO induces the relaxation of smooth muscle by increasing the cyclic GMP content. On the contrary, an inhibitor of soluble guanylate cyclase inhibited the NO-mediated increase in cyclic GMP content, whereas it did not affect NOmediated relaxation in the guinea pig and porcine trachea (10, 11), rat mesenteric artery (12) and canine aorta (13). Cyclic GMP-independent NO-mediated relaxation was also suggested in the gastrointestinal tract such as the rat duodenum (14) and proximal colon (15). There are also interesting reports that NO induces relaxation via cyclic GMPdependent and -independent mechanisms in the rat aorta (16) and NO induces relaxation via a cyclic GMP-independent mechanism in the rabbit aorta when the cyclic GMP-dependent protein kinase (PKG) system is blocked (17). These results indicate that the involvement of cyclic GMP in NO-mediated relaxation differs among animal species and tissues.The tension of the smooth muscle is mainly determined by the amount of phosphorylated myosin light chain (MLC), which is related to intracellular Ca

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Evidence that nitric oxide acts as an inhibitory neurotransmitter supplying taenia from the guinea‐pig caecum

Cited by 24 publications

References 31 publications

Involvement of nitric oxide and its up/down stream molecules in the immunity against parasitic infections

Involvement of nitric oxide and its up/down stream molecules in the immunity against parasitic infections

Mechanism of active repolarization of inhibitory junction potential in murine colon

Mechanism of a Nitric Oxide Donor NOR 1-Induced Relaxation in Longitudinal Muscle of Rat Proximal Colon

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