Somatostatin in the gut is expressed by both endocrine D cells and neurons. An implication of somatostatin in GI pain has been deduced from the ability of octreotide, a long-acting analog of somatostatin, to reduce the perception of gastric and rectal distension in healthy volunteers and IBS patients (37-43). Since octreotide increases discomfort thresholds in IBS patients, but not controls, at baseline and during experimentally induced hyperalgesia, it has been proposed that octreotide exerts primarily an antihyperalgesic rather than an analgesic effect (43). This effect could take place both at a peripheral and at a central site of action. Thus, somatostatin sst2 receptor activation by octreotide inhibits the activity of chemo- and mechan-osensitive spinal afferent nerve fibers innervating the rat jejunum (44), and the heptapeptide analog of somatostatin, TT-232, inhibits phenylquinone-induced writhing by a peripheral site of action (45). On the other hand, mechanonociception in the rat colon is inhibited by octreotide via a target within the spinal cord (46).
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