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Lubiprostone Stimulates HCO 3 − Secretion in Rat Stomach and Duodenum mediated by Different EP receptor Subtypes
Author(s) -
Takeuchi Koji
Publication year - 2016
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.30.1_supplement.720.1
Subject(s) - duodenum , lubiprostone , medicine , endocrinology , stomach , receptor antagonist , secretion , receptor , chemistry , antagonist , biology , chronic constipation , constipation
A recent study showed that lubiproston, a bicyclic fatty acid derived from prostaglandin (PG) E1, stimulated CFTR‐dependent duodenal HCO 3 − secretion in rat, and this action was mediated by the activation of EP4 receptors. In the present study, we examined the stimulatory effect of lubiprostone on HCO 3 − secretion in the rat stomach and duodenum, focusing on the EP receptor subtypes involved in this action. Male SD rats were used after 18 h fasting. Under urethane anesthesia, an ex‐vivo chambered stomach or a duodenal loop was perfused with saline, and HCO 3 − secretion was measured using a pH stat‐method. lubiprostone significantly increased HCO 3 − secretion in both the stomach (>30 μM) and duodenum (>1 μM). The stimulatory action in the stomach was significantly abrogated by prior administration of the EP1 antagonist but not by the EP3/EP4 antagonists or the CFTR inhibitor, while that in the duodenum was significantly attenuated by the EP3 antagonist and the EP4 antagonist as well as the CFTR inhibitor. These results suggest that lubiprostone stimulates HCO 3 − secretion in the stomach and duodenum mediated by different EP receptor subtypes; the former mediated by EP1 receptors and the latter mediated by both EP3 and EP4 receptors. It is also assumed that CFTR is involved in modulating HCO 3 − secretion in the duodenum but not the stomach Support or Funding Information None