Jin J G, Nakayama S
Department of Physiology, Okayama University Medical School, Japan.
Neurosci Lett. 1990 Feb 5;109(1-2):88-91. doi: 10.1016/0304-3940(90)90542-h.
In the isolated guinea-pig ileum, exposure to the sensory stimulant drug capsaicin (1 microM) produced a contraction thought to involve substance P(SP) release from sensory nerves. Bile salt, sodium deoxycholate, potentiated the capsaicin-induced contraction in a concentration-dependent (0.03-10 microM) manner, without influencing contractions produced by exogenous SP or by electrical stimulation of efferent nerves. The bile salt-induced potentiation of the capsaicin response was not modified by hexamethonium or indomethacin. It was, however, abolished by concomitant incubation with Ruthenium Red, which was reported to block transmembrane calcium fluxes and then suppress the SP release from the capsaicin-sensitive sensory nerve terminals. We propose that bile salt, as a calcium ionophore, could activate or sensitize the action of capsaicin on the peripheral terminals of sensory nerves.
在离体豚鼠回肠中,暴露于感觉刺激药物辣椒素(1微摩尔)会产生一种收缩,这种收缩被认为涉及感觉神经释放P物质(SP)。胆盐,即脱氧胆酸钠,以浓度依赖性(0.03 - 10微摩尔)的方式增强辣椒素诱导的收缩,而不影响外源性SP或传出神经电刺激所产生的收缩。胆盐诱导的辣椒素反应增强不受六甲铵或吲哚美辛的影响。然而,与钌红共同孵育可消除这种增强作用,据报道钌红可阻断跨膜钙通量,进而抑制辣椒素敏感感觉神经末梢释放SP。我们提出,胆盐作为一种钙离子载体,可激活或敏化辣椒素对感觉神经外周末梢的作用。