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EP1 and EP4 Receptors Mediate Exocytosis Evoked by Prostaglandin E 2 in Guinea‐Pig Antral Mucous Cells
Author(s) -
Ohnishi Atsuko,
Shimamoto Chikao,
Katsu Kenichi,
Ito Sigenori,
Imai Yusuke,
Nakahari Takashi
Publication year - 2001
Publication title -
experimental physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.925
H-Index - 101
eISSN - 1469-445X
pISSN - 0958-0670
DOI - 10.1113/eph8602160
Subject(s) - forskolin , agonist , stimulation , medicine , endocrinology , exocytosis , receptor , chemistry , prostaglandin e , prostaglandin , prostaglandin e2 receptor , biology , secretion
Effects of prostaglandin E 2 (PGE 2 ) on exocytosis of mucin were studied in mucous cells isolated from guinea‐pig antrum using video‐microscopy. Stimulation with PGE 2 elicited a sustained increase in the frequency of exocytotic events in a dose‐dependent manner, which was under regulation by both Ca 2+ and cAMP. Stimulation with a selective prostanoid EP4 receptor agonist (ONO‐AEI‐329, 10 μM), which activates cAMP signals, elicited a sustained increase in the frequency of exocytotic events (30% of that evoked by 1 μM PGE 2 ). Stimulation with an EP1 agonist (17‐P‐T‐PGE 2 , 1 μM), which activates Ca 2+ signals, increased the frequency of exocytotic events to a lesser extent (5% of that evoked by 1 μM PGE 2 ), while addition of an EP1 antagonist (ONO‐8713, 10 μM) decreased the frequency of exocytotic events (approximately 40% of that evoked by 1 μM PGE 2 ). However, addition of the EP1 agonist potentiated the frequency of exocytotic events evoked by the EP4 agonist or forskolin (which elevates cAMP levels) and increased the sensitivity of the exocytotic events to forskolin. These results suggest that the Ca 2+ signal activated via the EP1 receptor potentiates the cAMP‐regulated exocytotic events activated via the EP4 receptor during PGE 2 stimulation, by increasing the sensitivity of the exocytotic response to cAMP. In conclusion, exocytotic events in PGE 2 ‐stimulated antral mucous cells were regulated by interactions between EP1 and EP4 receptors.