Viscero‐somatic reflexes in referred pain areas evoked by capsaicin stimulation of the human gut

Arendt-Nielsen, Lars; Schipper, Klaus-Peter; Dimcevski, Georg; Sumikura, Hiroyuki; Krarup, Anne Lund; Giamberardino, Maria Adele; Drewes, Asbjørn Mohr

doi:10.1016/j.ejpain.2007.08.010

Cited by 47 publications

(29 citation statements)

References 38 publications

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“…hypertonic saline) (27,29,30). There is so far no description of BF changes in deep craniofacial tissues following nociceptive stimulation with capsaicin in contrast to abundant reports with increases in cutaneous BF, i.e., neurogenic inflammation (31-34) after topical or subcutaneous injection of capsaicin (14,19,20,(35)(36)(37)(38).…”

Section: Introductionmentioning

confidence: 80%

Effect of capsaicin-evoked jaw-muscle pain on intramuscular blood-flow

Arima

Arendt-Nielsen

Minagi

et al. 2009

Archives of Oral Biology

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Section: Introductionmentioning

confidence: 80%

Effect of capsaicin-evoked jaw-muscle pain on intramuscular blood-flow

Arima

Arendt-Nielsen

Minagi

et al. 2009

Archives of Oral Biology

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“…Not surprisingly, capsaicin induced pain and burning in all but one participant, which were presumably related to the activation of TRPV1-positive afferents in the duodenal mucosa, although non-TRPV1-mediated taste responses have been described previously in animals (30). The intestinal infusion of capsaicin has been used in several studies to induce pain (31)(32)(33)(34). Capsaicin has extensively been studied in models of experimental pain, and earlier studies have acutely applied capsaicin to the small intestine, which produced an evident pain response.…”

Section: Discussionmentioning

confidence: 99%

Capsaicin-induced satiety is associated with gastrointestinal distress but not with the release of satiety hormones

Avesaat

Troost

Westerterp-Plantenga

et al. 2016

The American Journal of Clinical Nutrition

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Background: Capsaicin, which is the major pungent principle in chili peppers, is able to induce satiety and reduce caloric intake. The exact mechanism behind this satiating effect is still unknown. We hypothesized that capsaicin induces satiety through the release of gastrointestinal peptides, such as glucagon-like peptide-1 (GLP-1) and peptide YY (PYY), from enteroendocrine cells in the small intestine. Objective: We investigate the effects of an intraduodenal capsaicin infusion (1.5 mg pure capsaicin) in healthy volunteers on hunger, satiety, and gastrointestinal symptoms and the release of GLP-1 and PYY. Design: Thirteen participants (7 women) [mean 6 SEM age: 21.5 6 0.6 y; body mass index (in kg/m 2 ): 22.8 6 0.6] participated in this single-blind, randomized, placebo-controlled crossover study with 2 different treatments. During test days, an intraduodenal infusion of either capsaicin or a placebo (physiologic saline) was performed with the use of a nasoduodenal catheter over a period of 30 min. Visual analog scale scores were used to measure hunger, satiety, and gastrointestinal symptoms. Blood samples were drawn at regular intervals for GLP-1 and PYY. Gallbladder volumes were measured with the use of real-time ultrasonography. Results: The intraduodenal capsaicin infusion significantly increased satiety (P-treatment effect , 0.05) but also resulted in an increase in the gastrointestinal symptoms pain (P-treatment 3 time interaction , 0.0005), burning sensation (P-treatment 3 time interaction , 0.0001), nausea (P-treatment 3 time interaction , 0.05), and bloating (P-treatment 3 time interaction , 0.001) compared with the effects of the placebo infusion. Satiety scores had a positive correlation with all gastrointestinal symptoms. No differences in GLP-1 and PYY concentrations and gallbladder volumes were observed after the capsaicin infusion compared with after the placebo infusion. Conclusions: An intraduodenal infusion of capsaicin significantly increases satiety but does not affect plasma concentrations of GLP-1 and PYY. Rather, the effect on satiety seems related to gastrointestinal stress as shown by the associations with pain, burning sensation, nausea, and bloating scores. This trial was registered at clinicaltrials.gov as NCT01667523.Am J Clin Nutr 2016;103:305-13.

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“…11,12 The intracolonic capsaicin model in mice may represent an appropriate translational model of visceral pain, because application of capsaicin to the human gut evokes intense (acute) pain and referred mechanical hyperalgesia and is a well-validated human model of visceral pain. [13][14][15] Sigma receptors have been classified into two distinct subtypes, sigma-1 (σ 1 ) and sigma-2 (σ 2 ), although only the σ 1 receptor has been cloned. 16,17 σ 1 Receptors are highly expressed in the central nervous system, including important areas for pain control such as the superficial layers of the spinal cord dorsal horn, periaqueductal gray matter, locus coeruleus, and rostroventral medulla.…”

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confidence: 99%

σ1Receptors Are Involved in the Visceral Pain Induced by Intracolonic Administration of Capsaicin in Mice

2013

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Background: Visceral pain is an important and prevalent clinical condition whose treatment is challenging. Sigma-1 (σ 1 ) receptors modulate somatic pain, but their involvement in pure visceral pain is unexplored. Methods: The authors evaluated the role of σ 1 receptors in intracolonic capsaicin-induced visceral pain (pain-related behaviors and referred mechanical hyperalgesia to the abdominal wall) using wild-type (WT) (n = 12 per group) and σ 1 receptor knockout (σ 1 -KO) (n = 10 per group) mice, selective σ 1 receptor antagonists (BD-1063, S1RA, and NE-100), and control drugs (morphine and ketoprofen). Results: The intracolonic administration of capsaicin (0.01-1%) induced concentration-dependent visceral pain-related behaviors and referred hyperalgesia in both WT and σ 1 -KO mice. However, the maximum number of pain-related behaviors induced by 1% capsaicin in σ 1 -KO mice (mean ± SEM, 22 ± 2.9) was 48% of that observed in WT animals (46 ± 4.2). Subcutaneous administration of the σ 1 receptor antagonists BD-1063 (16-64 mg/kg), S1RA (32-128 mg/kg), and NE-100 (8-64 mg/kg) dose-dependently reduced the number of behavioral responses (by 53, 62, and 58%, respectively) and reversed the referred hyperalgesia to mechanical control threshold (0.53 ± 0.05 g) in WT mice. In contrast, these drugs produced no change in σ 1 -KO mice. Thus, the effects of these drugs are specifically mediated by σ 1 receptors. Morphine produced an inhibition of capsaicin-induced visceral pain in WT and σ 1 -KO mice, whereas ketoprofen had no effect in either mouse type. Conclusion: These results suggest that σ 1 receptors play a role in the mechanisms underlying capsaicin-induced visceral pain and raise novel perspectives for their potential therapeutic value.

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Viscero‐somatic reflexes in referred pain areas evoked by capsaicin stimulation of the human gut

Cited by 47 publications

References 38 publications

Effect of capsaicin-evoked jaw-muscle pain on intramuscular blood-flow

Effect of capsaicin-evoked jaw-muscle pain on intramuscular blood-flow

Capsaicin-induced satiety is associated with gastrointestinal distress but not with the release of satiety hormones

σ1Receptors Are Involved in the Visceral Pain Induced by Intracolonic Administration of Capsaicin in Mice

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