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Vol. 108 (1996) No. 5 P 233-242



There are now abundant evidence to confirm the role of serotonin (5-HT) and in particular, 5-HT3 receptors in the control of cisplatin-induced emesis. Emesis caused by cisplatin is associated with an increase in the concentration of 5-HT in the intestinal mucosa and in the area postrema. The intestinal mucosa contains enterochromaffin (EC) cells that synthesize and secrete approximately 80% of all 5-HT produced in the body. A selective 5-HT3 agonist, 2-methyl-5-HT, induced a dose-dependent increase in 5-HT level from the ileum. Furthermore, a selective 5-HT4-receptor agonist, 5-methoxytryptamine also induced a concentration-dependent increase of 5-HT level. Both 5-HT3 and 5-HT4 receptors may be involved in intestinal 5-HT release. It is proposed that anticancer drugs cause 5-HT release from the EC cells and that the released 5-HT stimulates the 5-HT3 receptors on the afferent vagal fibers, resulting in their deporalization. Electrical stimulation of the abdominal vagal afferents is capable of inducing emesis, and abdominal vagotomy suppresses cisplatin-induced emesis. These results indicate that the vagus is the major afferent pathway involved in the detection of emetic stimuli.

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