Evidence for involvement of prostaglandin I2 as a major nociceptive mediator in acetic acid-induced writhing reaction: a study using IP-receptor disrupted mice.
Ohishi
S
S
Department of Pharmacology, School of Pharmaceutical Sciences, Kitasato University, Tokyo.
Ueno
A
A
Matsumoto
H
H
Murata
T
T
Ushikubi
F
F
Narumiya
S
S
D015121:6-Ketoprostaglandin F1 alpha / Q000378:metabolism; D019342:Acetic Acid / Q000633:toxicity; D018712:Analgesics, Non-Narcotic / Q000494:pharmacology; D000818:Animals; D001202:Ascitic Fluid / Q000378:metabolism; D015232:Dinoprostone / Q000378:metabolism; D011464:Epoprostenol / Q000502:physiology*; D007213:Indomethacin / Q000494:pharmacology; D008297:Male; D051379:Mice; D008813:Mice, Inbred ICR; D018345:Mice, Knockout; D009619:Nociceptors / Q000187:drug effects / Q000502:physiology*; D010146:Pain / Q000139:chemically induced / Q000503:physiopathology*; D010147:Pain Measurement; D044006:Receptors, Epoprostenol; D011982:Receptors, Prostaglandin / Q000187:drug effects / Q000235:genetics / Q000502:physiology*
D018712:Analgesics, Non-Narcotic; D044006:Receptors, Epoprostenol; D011982:Receptors, Prostaglandin; D015121:6-Ketoprostaglandin F1 alpha; D011464:Epoprostenol; D015232:Dinoprostone; D019342:Acetic Acid; D007213:Indomethacin