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Monochloramine effects on gallbladder contractility.

David Hernández-Moreno1, Sara Morales2, Cristina Camello-Almaraz2

  • 1Department of Environment and Agronomy, National Institute for Agricultural and Food Research and Technology (INIA), Madrid, Spain.

Clinical and Experimental Pharmacology & Physiology
|December 22, 2020
PubMed
Summary
This summary is machine-generated.

Monochloramine, an oxidant found in digestive inflammation, causes gallbladder contractions by activating tyrosine kinase, protein kinase C (PKC), and mitogen-activated protein kinase (MAPK) pathways. This oxidant also impairs gallbladder responses to cholecystokinin (CCK) and nerve stimulation.

Keywords:
gallbladder motilitymonochloraminereactive oxygen speciessignal transduction pathwayssmooth muscle

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Area of Science:

  • Gastroenterology
  • Cellular Physiology
  • Oxidative Stress Research

Background:

  • Digestive inflammation is linked to altered gut motility and increased reactive oxygen species (ROS).
  • Monochloramine (NH2Cl) is a naturally occurring oxidant implicated in these processes.
  • Understanding NH2Cl's role in gallbladder function is crucial for inflammatory bowel disease research.

Purpose of the Study:

  • To characterize the in vitro effects of monochloramine (NH2Cl) on guinea pig gallbladder contractility.
  • To elucidate the signaling pathways involved in NH2Cl-induced gallbladder contractions.
  • To investigate NH2Cl's impact on gallbladder responses to physiological stimuli.

Main Methods:

  • Standard in vitro contractility technique was employed on guinea pig gallbladder strips.
  • Concentration-dependent contractions induced by NH2Cl were measured.
  • The effects of various inhibitors (tyrosine kinase, PKC, MAPK, NOS, PLA2, COX) and stimuli (Ca2+ influx, CCK, depolarization, EFS) were assessed.

Main Results:

  • NH2Cl induced concentration-dependent contractions in gallbladder strips.
  • These contractions were mediated by extracellular Ca2+ influx, tyrosine kinase, protein kinase C (PKC), mitogen-activated protein kinase (MAPK), nitric oxide synthase (NOS), phospholipase A2 (PLA2), and cyclooxygenase (COX) pathways.
  • NH2Cl significantly impaired gallbladder responses to cholecystokinin (CCK), tissue depolarization, and electrical field stimulation (EFS).

Conclusions:

  • Monochloramine directly induces gallbladder contractions via complex signaling cascades involving tyrosine kinase, PKC, MAPK, and NO pathways.
  • NH2Cl impairs gallbladder function by affecting responses to CCK, membrane depolarization, and neural stimulation.
  • These findings highlight monochloramine's detrimental role in gallbladder motility during digestive inflammatory processes.