Abstract
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.
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