Role of nitric oxide in esophageal peristalsis in the opossum

Yamato, Shigeru; Spechler, Stuart J.; Goyal, Raj K.

doi:10.1016/0016-5085(92)91113-i

Cited by 164 publications

(99 citation statements)

References 18 publications

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“…The other contraction occurred after stimulus and was called the "B wave." NOS inhibitors strongly increased the velocity of the cholinergic A wave by decreasing the time of its arrival in the distal esophagus (38), a very similar result to what we found on latency in the human EB. Animal studies also found that the amplitude of esophageal peristalsis is controlled by a peripherally located gradient of cholinergic innervation, most prominent proximally, and which decreases distally along the smooth muscle portion of the esophagus (5).…”

Section: Discussionsupporting

confidence: 88%

Regional functional specialization and inhibitory nitrergic and nonnitrergic coneurotransmission in the human esophagus

Lecea

Gallego

Farré

et al. 2011

American Journal of Physiology-Gastrointestinal and Liver Physi

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Lecea B, Gallego D, Farré R, Opazo A, Aulí M, Jiménez M, Clavé P. Regional functional specialization and inhibitory nitrergic and nonnitrergic coneurotransmission in the human esophagus. Am J Physiol Gastrointest Liver Physiol 300: G782-G794, 2011. First published February 17, 2011 doi:10.1152/ajpgi.00514.2009.-The aim of this study was to explore the myenteric mechanisms of control of human esophageal motility and the effect of nitrergic and nonnitrergic neurotransmitters. Human circular esophageal strips were studied in organ baths and with microelectrodes. Responses following electrical field stimulation (EFS) of enteric motoneurons (EMNs) or through nicotinic acetylcholine receptors were compared in the esophageal body (EB) and in clasp and sling regions in the lower esophageal sphincter (LES). In clasp LES strips: 1) sodium nitroprusside (1 nM to 100 M), adenosine-5=-[␤-thio]diphosphate trilithium salt (1-100 M), and vasoactive intestinal peptide (1 nM to 1 M) caused a relaxation; 2) 1 mM N -nitro-L-arginine (L-NNA) shifted the EFS "on"-relaxation to an "off"-relaxation, partly antagonized by 10 M 2=-deoxy-N 6 -methyladenosine 3=,5=-bisphosphate tetrasodium salt (MRS2179) or 10 U/ml ␣-chymotrypsin; and 3) nicotine-relaxation (100 M) was mainly antagonized by L-NNA, and only partly by MRS2179 or ␣-chymotrypsin. In sling LES fibers, EFS and nicotine relaxation was abolished by L-NNA. In the EB, L-NNA blocked the latency period, and MRS2179 reduced "off"-contraction. The amplitude of cholinergic contraction decreased from the EB to both LES sides. EFS induced a monophasic inhibitory junction potential in clasp, sling, and EB fibers abolished by L-NNA. Our study shows a regional specialization to stimulation of EMNs in the human esophagus, with stronger inhibitory responses in clasp LES fibers and stronger cholinergic excitatory responses in the EB. Inhibitory responses are mainly triggered by nitrergic EMNs mediating the inhibitory junction potentials in the LES and EB, EFS on-relaxation in clasp and sling LES sides, and latency in the EB. We also found a minor role for purines (through P2Y1 receptors) and vasoactive intestinal peptide-mediating part of nonnitrergic clasp LES relaxation. lower esophageal sphincter; esophageal body; inhibitory motoneurons; inhibitory coneurotransmission THE MAIN PHYSIOLOGICAL FUNCTION of the lower esophageal sphincter (LES) is to generate a zone of high pressure that prevents the reflux of acid gastric content into the esophagus. LES relaxations occur briefly after swallowing, and transient LES relaxations cause physiological gastroesophageal reflux and allow belching. Enteric motoneurons (EMNs) are the final step in the inhibitory vagal pathway to the LES, mediating swallow-induced and transient LES relaxation (3). Nitric oxide (NO) released from these inhibitory EMNs is the major contributor to LES relaxation in humans (12) and opossums (20, 33). However, vasoactive intestinal peptide (VIP) and ATP are putative inhibitory neurotransmitters in animal studies (14, 21-24, 34, ...

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Section: Discussionsupporting

confidence: 88%

Regional functional specialization and inhibitory nitrergic and nonnitrergic coneurotransmission in the human esophagus

Lecea

Gallego

Farré

et al. 2011

American Journal of Physiology-Gastrointestinal and Liver Physi

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“…The incidence of various patterns of responses by EFS in esophageal smooth muscle in vitro, which are composed of on-and off-contractions, differ at esophageal sites and are dependent on stimulation frequencies. These events result from the influence of the integration of intramural excitatory cholinergic and NANC inhibitory nitrergic nerves, which innervate esophageal smooth muscle [4,11]. In addition, ion currents generated via 4-AP-sensitive voltage-dependent K ＋ channels in muscle might participate in EFS-induced responses [12].…”

Section: Introductionmentioning

confidence: 99%

MLCK and PKC Involvements via Gi and Rho A Protein in Contraction by the Electrical Field Stimulation in Feline Esophageal Smooth Muscle

Park

Shim

Kim

et al. 2010

Korean J Physiol Pharmacol

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W e have shown that myosin light chain kinase (MLCK) was required for the off-contraction in response to the electrical field stimulation (EFS) of feline esophageal smooth muscle. In this study, we investigated whether protein kinase C (PKC) may require the on-contraction in response to EFS using feline esophageal smooth muscle. The contractions were recorded using an isometric force transducer. On-contraction occurred in the presence of N G -nitro-L-arginine methyl ester (L-NAME), suggesting that nitric oxide acts as an inhibitory mediator in smooth muscle. The excitatory composition of both contractions was cholinergic dependent which was blocked by tetrodotoxin or atropine. The on-contraction was abolished in Ca 2＋ -free buffer but reappeared in normal Ca 2＋ -containing buffer indicating that the contraction was Ca 2＋ dependent. 4-aminopyridine (4-AP), voltage-dependent K＋ channel blocker, significantly enhanced on-contraction. Aluminum fluoride (a G-protein activator) increased on-contraction. Pertussis toxin (a Gi inactivator) and C3 exoenzyme (a rhoA inactivator) significantly decreased on-contraction suggesting that Gi or rhoA protein may be related with Ca 2＋ and K ＋ channel. ML-9, a MLCK inhibitor, significantly inhibited on-contraction, and chelerythrine (PKC inhibitor) affected on the contraction. These results suggest that endogenous cholinergic contractions activated directly by low-frequency EFS may be mediated by Ca 2＋ , and G proteins, such as Gi and rhoA, which resulted in the activation of MLCK, and PKC to produce the contraction in feline distal esophageal smooth muscle.

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“…This activation probably occurs through release of intracellular calcium via an M3 pathway and has the potential to modulate the timing and amplitude of peristaltic contraction along the esophagus. esophagus; acetylcholine; potassium channel REGIONAL DIFFERENCES IN NEURAL influence have been described along the circular smooth muscle esophageal body (EB), including the excitatory (cholinergic) influence most prominent proximally (5, 8 -10, 12, 30), and the inhibitory (nitrergicnitric oxide) influence most active distally (2,11,40,41). Hence, peristaltic contractions are considered to be the result of the local muscle responding passively to neural signals.…”

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confidence: 99%

Regional differences in cholinergic regulation of potassium current in feline esophageal circular smooth muscle

Muinuddin¹,

Naqvi²,

Sheu³

et al. 2005

American Journal of Physiology-Gastrointestinal and Liver Physi

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Potassium channels are important contributors to membrane excitability in smooth muscles. There are regional differences in resting membrane potential and K ϩ -channel density along the length of the feline circular smooth muscle esophagus. The aim of this study was to assess responses of K ϩ -channel currents to cholinergic (ACh) stimulation along the length of the feline circular smooth muscle esophageal body. Perforated patchclamp technique assessed K ϩ -channel responses to ACh stimulation in isolated smooth muscle cells from the circular muscle layer of the esophageal body at 2 (distal)-and 4-cm (proximal) sites above the lower esophageal sphincter. Western immunoblots assessed ion channel and receptor expression. ACh stimulation produced a transient increase in outward current followed by inhibition of spontaneous transient outward currents. These ACh-induced currents were abolished by blockers of large-conductance Ca 2ϩ -dependent K ϩ channels (BKCa). Distal cells demonstrated a greater peak current density in outward current than cells from the proximal region and a longerlasting outward current increase. These responses were abolished by atropine and the specific M3 receptor antagonist 4-DAMP but not the M1 receptor antagonist pirenzipine or the M2 receptor antagonist methoctramine. BKCa expression along the smooth muscle esophagus was similar, but M3 receptor expression was greater in the distal region. Therefore, ACh can differentially activate a potassium channel (BKCa) current along the smooth muscle esophagus. This activation probably occurs through release of intracellular calcium via an M3 pathway and has the potential to modulate the timing and amplitude of peristaltic contraction along the esophagus.

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Role of nitric oxide in esophageal peristalsis in the opossum

Cited by 164 publications

References 18 publications

Regional functional specialization and inhibitory nitrergic and nonnitrergic coneurotransmission in the human esophagus

Regional functional specialization and inhibitory nitrergic and nonnitrergic coneurotransmission in the human esophagus

MLCK and PKC Involvements via Gi and Rho A Protein in Contraction by the Electrical Field Stimulation in Feline Esophageal Smooth Muscle

Regional differences in cholinergic regulation of potassium current in feline esophageal circular smooth muscle

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