Because of the finding that a 25-mg/kg dose of 5-hydroxytryptophan (5-HTP) causes stressful behavior in eliciting an increase in canine GH (cGH) and corticosteroid levels, we compared it to the stimulatory action of another stress, insulininduced hypoglycemia. In five unanesthetized adult bitches given an iv injection of insulin, there was a rapid fall in blood glucose (from 77 to 25 mg/dl at 30 min), with increases in both corticosteroid and cGH concentrations (of 17.1 μg/dl and 7.9 ng/ml, respectively, at 60 min). Pentobarbital anesthesia (30 mg/kg) did not modify the decrease in glucose after insulin administration, although it abolished the increases in corticosteroids and cGH concentrations. 5-HTP (25 mg/kg) produced significant increments in plasma cGH in pentobarbital-anesthetized animals, although it failed to stimulate corticosteroids. This failure of pentobarbital to modify the cGH response to 5-HTP suggests that the serotoninergic mechanism of stimulation may differ from the stress-related mehanism of cGH release. Inhibition of peripheral 5-HTP conversion to serotonin with carbidopa was measured in five animals. It was observed that the 1-mg/kg 5-HTP-induced rise in cGH was converted from an early to a late response with inhibition of peripheral decarboxylation. The rapid cGH increases resulting from low dose 5-HTP stimulation along with an absence of both behavioral distress and increases in corticoids suggest that serotoninergic stimulation may have peripheral as well as central activity. Studies of animals with direct injections of serotonin have thus far failed to confirm this hypothesis.
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