Nakao K, Kitamura K, Kuriyama H
Department of Pharmacology, Faculty of Medicine, Kyushu University, Fukuoka, Japan.
Am J Physiol. 1989 Jan;256(1 Pt 1):G100-6. doi: 10.1152/ajpgi.1989.256.1.G100.
Effects of prostaglandin E2, F2 alpha, and synthetic thromboxane A2 (PGE2, PGF2 alpha, and STA2, respectively) on electrical and mechanical responses of the rabbit cecum were investigated. Transmural electrical stimulation evoked an excitatory junction potential (EJP) and contraction, events that were inhibited by 1 microM atropine or 0.3 microM tetrodotoxin. Indomethacin (up to 30 microM) modified neither the membrane potential nor the muscle tone but did inhibit amplitudes of the EJP and the twitch contraction. In the presence of 30 microM indomethacin, PGE2 (below 1 nM) had no effect on the membrane potential or muscle tone, while PGE2 (above 10 nM) contracted the cecal tissues, without depolarization. PGE2 enhanced the twitch contraction and restored the EJP in the presence of 30 microM indomethacin. Acetylcholine (0.1-3 microM) depolarized the membrane, but in the presence of 30 microM indomethacin, this depolarization was inhibited. PGE2 (0.1-100 nM) prevented these inhibitory actions of indomethacin. PGF2 alpha (0.1-100 nM) had weaker actions than PGE2 while STA2 (0.1-100 nM) had no effect on muscarinic responses. Thus muscarinic responses are augmented by primary prostaglandins.
研究了前列腺素E2、F2α和合成血栓素A2（分别为PGE2、PGF2α和STA2）对兔盲肠电反应和机械反应的影响。透壁电刺激可诱发兴奋性接头电位（EJP）和收缩，这些反应可被1μM阿托品或0.3μM河豚毒素抑制。吲哚美辛（高达30μM）既不改变膜电位也不改变肌张力，但可抑制EJP和抽搐收缩的幅度。在存在30μM吲哚美辛的情况下，PGE2（低于1 nM）对膜电位或肌张力无影响，而PGE2（高于10 nM）可使盲肠组织收缩，且无去极化现象。在存在30μM吲哚美辛的情况下，PGE2可增强抽搐收缩并恢复EJP。乙酰胆碱（0.1 - 3μM）使膜去极化，但在存在30μM吲哚美辛的情况下，这种去极化受到抑制。PGE2（0.1 - 100 nM）可阻止吲哚美辛的这些抑制作用。PGF2α（0.1 - 100 nM）的作用比PGE2弱，而STA2（0.1 - 100 nM）对毒蕈碱反应无影响。因此，原发性前列腺素可增强毒蕈碱反应。
