Adenosine modulates oesophageal sensorimotor function in humans

Troche, José María Remes; Chahal, Premjit S.; Mudipalli, Ranjit; Rao, Satish S.

doi:10.1136/gut.2006.116699

Cited by 18 publications

(16 citation statements)

References 59 publications

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“…A moderate sensitizing effect of the adenosine receptors stimulation may also contribute to the overall nociceptive activity to evoke chest pain. Consistent with this notion, infusion of adenosine in relatively low doses reduced the mechanical pain threshold (33), and higher doses of adenosine were required to induce transient chest pain (36,39).…”

Section: Discussionmentioning

confidence: 88%

“…It is also probable that, similar to the neighboring respiratory system in which vagal nociceptors (bronchopulmonary C fibers) modulate regulatory reflexes (10,24), vagal esophageal nociceptors may modulate the reflex regulation of the esophagus. In this context, it is noteworthy that certain esophageal muscle function abnormalities noted in patients with functional chest pain (increase in the esophageal wall stiffness and increase in the cross-sectional area) can be mimicked by adenosine (26,33). Although these effects on esophageal muscle may be due to local actions of adenosine in the esophageal wall, it is tempting to speculate that the modulation of esophageal motor reflexes mediated by vagal nociceptors also contributes to these effects.…”

Section: Discussionmentioning

confidence: 91%

“…Intravenous adenosine induced esophageal hyperalgesia (33) similar to that observed in many patients with functional chest pain (26). Specifically, adenosine lowered the mechanical threshold for pain evoked by esophageal distention, indicating that adenosine influences esophageal nociceptive pathways (33). In high doses, intravenous adenosine induced chest discomfort and pain (36,39) that was reduced by the methylxanthine nonselective adenosine receptor antagonist aminophylline (36).…”

mentioning

confidence: 93%

“…1 and 8). Intravenous adenosine induced esophageal hyperalgesia (33) similar to that observed in many patients with functional chest pain (26). Specifically, adenosine lowered the mechanical threshold for pain evoked by esophageal distention, indicating that adenosine influences esophageal nociceptive pathways (33).…”

mentioning

confidence: 95%

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Adenosine-induced activation of esophageal nociceptors

Ren

Surdenikova

Brozmanová

et al. 2011

American Journal of Physiology-Gastrointestinal and Liver Physi

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Clinical studies implicate adenosine acting on esophageal nociceptive pathways in the pathogenesis of noncardiac chest pain originating from the esophagus. However, the effect of adenosine on esophageal afferent nerve subtypes is incompletely understood. We addressed the hypothesis that adenosine selectively activates esophageal nociceptors. Whole cell perforated patch-clamp recordings and single-cell RT-PCR analysis were performed on the primary afferent neurons retrogradely labeled from the esophagus in the guinea pig. Extracellular recordings were made from the isolated innervated esophagus. In patch-clamp studies, adenosine evoked activation (inward current) in a majority of putative nociceptive (capsaicin-sensitive) vagal nodose, vagal jugular, and spinal dorsal root ganglia (DRG) neurons innervating the esophagus. Single-cell RT-PCR analysis indicated that the majority of the putative nociceptive (transient receptor potential V1-positive) neurons innervating the esophagus express the adenosine receptors. The neural crest-derived (spinal DRG and vagal jugular) esophageal nociceptors expressed predominantly the adenosine A(1) receptor while the placodes-derived vagal nodose nociceptors expressed the adenosine A(1) and/or A(2A) receptors. Consistent with the studies in the cell bodies, adenosine evoked activation (overt action potential discharge) in esophageal nociceptive nerve terminals. Furthermore, the neural crest-derived jugular nociceptors were activated by the selective A(1) receptor agonist CCPA, and the placodes-derived nodose nociceptors were activated by CCPA and/or the selective adenosine A(2A) receptor CGS-21680. In contrast to esophageal nociceptors, adenosine failed to stimulate the vagal esophageal low-threshold (tension) mechanosensors. We conclude that adenosine selectively activates esophageal nociceptors. Our data indicate that the esophageal neural crest-derived nociceptors can be activated via the adenosine A(1) receptor while the placodes-derived esophageal nociceptors can be activated via A(1) and/or A(2A) receptors. Direct activation of esophageal nociceptors via adenosine receptors may contribute to the symptoms in esophageal diseases.

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Section: Discussionmentioning

confidence: 88%

Section: Discussionmentioning

confidence: 91%

mentioning

confidence: 93%

mentioning

confidence: 95%

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Adenosine-induced activation of esophageal nociceptors

Ren

Surdenikova

Brozmanová

et al. 2011

American Journal of Physiology-Gastrointestinal and Liver Physi

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“…Recently, our group showed that adenosine can induce visceral hyperalgesia and decrease esophageal distensibility in healthy humans, serving as a key neuromediator in the pathogenesis of functional chest pain [36]. In a further, double-blind, randomized, placebo-controlled study, 20 patients with functional chest pain of presumed esophageal origin (Rome III criteria) received either adenosine or placebo infusion intravenously at a rate of 100 μg/kg/min [37].…”

Section: Peripheral Sensitizationmentioning

confidence: 99%

The Hypersensitive Esophagus: Pathophysiology, Evaluation, and Treatment Options

Troche

2010

Curr Gastroenterol Rep

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Visceral hypersensitivity plays a key role in the pathogenesis of esophageal functional disorders such as functional heartburn and chest pain of presumed esophageal origin (noncardiac chest pain). About 80% of patients with unexplained noncardiac chest pain exhibit lower esophageal sensory thresholds when compared to controls during esophageal sensory testing (ie, esophageal barostat, impedance planimetry). Such information has led to prescription of peripherally and/or centrally acting therapies for the management of these patients. This review summarizes and highlights recent and significant findings regarding the pathophysiology, evaluation, and treatment of the hypersensitive esophagus, a central factor in functional esophageal disorders.

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Non‐Cardiac Chest Pain

Fass

Herschcovici

2012

The Esophagus

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Adenosine modulates oesophageal sensorimotor function in humans

Cited by 18 publications

References 59 publications

Adenosine-induced activation of esophageal nociceptors

Adenosine-induced activation of esophageal nociceptors

The Hypersensitive Esophagus: Pathophysiology, Evaluation, and Treatment Options

Non‐Cardiac Chest Pain

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