Trypsin-induced biphasic regulation of tone in the porcine lower esophageal sphincter

Tanaka, Yoshimasa; Ihara, Eikichi; Hirano, Katsuya; Takahashi, Shunsuke; Hirano, Minoru; Nakamura, Kazuhiko; Akiho, Hirotada; Oda, Yoshinao; Takayanagi, Ryoichi

doi:10.1016/j.ejphar.2015.02.008

Cited by 3 publications

(1 citation statement)

References 29 publications

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“…TRPV1 releases substance P (SP), which activates natural killer receptors (NKR) 1/2 to induce contraction in CSM [57]. Tanaka et al [58] concluded that PAR-2 induces the activation of Rho-associated protein kinase (ROK), p38 mitogen-activated protein kinase (p38 MAPK) and extracellular signal-regulated protein kinase (ERK) 1/2. ROK is involved in the contractile function of CSM, whereas ROK, p38 MAPK, ERK1/2, and membrane hyperpolarization are involved in relaxation.…”

Section: Trypsinmentioning

confidence: 99%

Effects of acids, pepsin, bile acids, and trypsin on laryngopharyngeal reflux diseases: physiopathology and therapeutic targets

Zhou

et al. 2021

Eur Arch Otorhinolaryngol

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Purpose Laryngopharyngeal reflux disease (LPRD) is a general term for the reflux of gastroduodenal contents into the laryngopharynx, oropharynx and even the nasopharynx, causing a series of symptoms and signs. Currently, little is known regarding the physiopathology of LPRD, and proton pump inhibitors (PPIs) are the drugs of choice for treatment. Although acid reflux plays a critical role in LPRD, PPIs fail to relieve symptoms in up to 40% of patients with LPRD. The influence of other reflux substances on LPRD, including pepsin, bile acid, and trypsin, has received increasing attention. Clarification of the substances involved in LPRD is the basis for LPRD treatment. Methods A review of the effects of acids, pepsin, bile acids, and trypsin on laryngopharyngeal reflux diseases was conducted in PubMed. Results Different reflux substances have different effects on LPRD, which will cause various symptoms, inflammatory diseases and neoplastic diseases of the laryngopharynx. For LPRD caused by different reflux substances, 24-h multichannel intraluminal impedance combined with pH-metry (MII-pH), salivary pepsin, bile acid and other tests should be established so that different drugs and treatment courses can be used to provide patients with more personalized treatment plans. Conclusion This article summarizes the research progress of different reflux substances on the pathogenesis, detection index and treatment of LPRD and lays a theoretical foundation to develop target drugs and clinical diagnosis and treatment.

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Section: Trypsinmentioning

confidence: 99%

Effects of acids, pepsin, bile acids, and trypsin on laryngopharyngeal reflux diseases: physiopathology and therapeutic targets

Zhou

et al. 2021

Eur Arch Otorhinolaryngol

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Trypsin induces biphasic muscle contraction and relaxation via transient receptor potential vanilloid 1 and neurokinin receptors 1/2 in porcine esophageal body

Bai

Tanaka

Ihara

et al. 2017

European Journal of Pharmacology

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Duodenal reflux of fluids containing trypsin relates to refractory gastroesophageal reflux disease (GERD). Esophageal peristalsis and clearance are important factors in GERD pathogenesis. However, the function of trypsin in esophageal body contractility is not fully understood. In this study, effects of trypsin on circular smooth muscle (CSM) and longitudinal smooth muscle (LSM) of the porcine esophageal body were examined. Trypsin elicited a concentration dependent biphasic response, a major contraction and a subsequent relaxation only in CSM. In CSM, contraction occurred at trypsin concentrations of 100nM and relaxation at 1μM. A proteinase-activated receptor (PAR)2 activating peptide, SLIGKV-NH (1mM), induced a monophasic contraction. Those responses were unaffected by tetrodotoxin though abolished by the gap junction uncouplers carbenoxolone and octanol. They were also partially inhibited by a transient receptor potential vanilloid type 1 (TRPV1) antagonist and abolished by combination of neurokinin receptor 1 (NK) and NK antagonists, but not by an NK antagonist, suggesting a PAR2-TRPV1-substance P pathway in sensory neurons. Substance P (100nM), an agonist for various NK receptors (NK, NK and NK) with differing affinities, induced significant contraction in CSM, but not in LSM. The contraction was also blocked by the combination of NK and NK antagonists, but not by the NK antagonist. Moreover, substance P-induced contractions were unaffected by the TRPV1 antagonist, but inhibited by a gap junction uncoupler. In conclusion, trypsin induced a biphasic response only in CSM and this was mediated by PAR2, TRPV1 and NK. Gap junctions were indispensable in this tachykinin-induced response.

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Trypsin-induced elevated contractile responses in a rat model of interstitial cystitis/bladder pain syndrome: Involvement of PAR2 and intracellular Ca2+ release pathways

et al. 2022

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Trypsin-induced biphasic regulation of tone in the porcine lower esophageal sphincter

Cited by 3 publications

References 29 publications

Effects of acids, pepsin, bile acids, and trypsin on laryngopharyngeal reflux diseases: physiopathology and therapeutic targets

Effects of acids, pepsin, bile acids, and trypsin on laryngopharyngeal reflux diseases: physiopathology and therapeutic targets

Trypsin induces biphasic muscle contraction and relaxation via transient receptor potential vanilloid 1 and neurokinin receptors 1/2 in porcine esophageal body

Trypsin-induced elevated contractile responses in a rat model of interstitial cystitis/bladder pain syndrome: Involvement of PAR2 and intracellular Ca2+ release pathways

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