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Monochloramine effects on gallbladder contractility
Author(s) -
HernándezMoreno David,
Morales Sara,
CamelloAlmaraz Cristina,
Pozo María J.,
Camello Pedro J.
Publication year - 2021
Publication title -
clinical and experimental pharmacology and physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.752
H-Index - 103
eISSN - 1440-1681
pISSN - 0305-1870
DOI - 10.1111/1440-1681.13453
Subject(s) - protein kinase c , endocrinology , medicine , contractility , chemistry , stimulation , tyrosine kinase , depolarization , protein kinase a , biology , kinase , signal transduction , biochemistry
Digestive inflammatory processes induce motility alterations associated with an increase in reactive oxygen species production, including monochloramine (NH 2 Cl). The aim of the study was to characterize the effects of the naturally occurring oxidant monochloramine in the guinea pig gallbladder. We used standard in vitro contractility technique to record guinea pig gallbladder strips contractions. NH 2 Cl caused a concentration‐dependent contraction which was reduced by inhibition of extracellular Ca 2+ influx and tyrosine kinase pathways. The PKC antagonist GF109203X also reduced the response but not after previous tyrosine kinase inhibition, suggesting that PKC is activated by tyrosine kinase activity. The NH 2 Cl contractile effect was also reduced by inhibitors of mitogen‐activated protein kinase (MAPK), nitric oxide synthase, phospholipase A2 and cyclooxygenase. In addition, NH 2 Cl impaired the responses to CCK, tissue depolarization and electrical field stimulation. In conclusion, we present new evidence that monochloramine impairs not only the gallbladder response to CCK but also to membrane depolarization and nervous plexus stimulation, and that tyrosine kinase, PKC, MAPK and NO pathways are involved in the contractile direct effect of monochloramine.