551. p-Chloroamphetamine, a serotonin-releasing drug, elicited in rats a hyperglycemia mediated by the 5-HT1A and 5-HT2B/2C receptors.
- Author
-
Yamada J, Sugimoto Y, and Yoshikawa T
- Subjects
- 4-Aminobenzoic Acid pharmacology, Adrenal Medulla physiology, Adrenalectomy, Aminopyridines pharmacology, Animals, Blood Glucose metabolism, Dose-Response Relationship, Drug, Ergolines pharmacology, Fenclonine pharmacology, Hyperglycemia physiopathology, Hyperglycemia prevention & control, Indoles pharmacology, Ketanserin pharmacology, Male, Methysergide pharmacology, Piperazines pharmacology, Propranolol pharmacology, Rats, Rats, Sprague-Dawley, Receptor, Serotonin, 5-HT2B, Receptor, Serotonin, 5-HT2C, Receptors, Serotonin, 5-HT1, Ritanserin pharmacology, Serotonin metabolism, Serotonin Antagonists pharmacology, Serotonin Antagonists therapeutic use, Tropisetron, para-Aminobenzoates, Blood Glucose drug effects, Hyperglycemia chemically induced, Receptors, Serotonin physiology, Serotonin Agents pharmacology, p-Chloroamphetamine pharmacology
- Abstract
The effects of a serotonin (5-HT) releasing drug, p-chloroamphetamine, on plasma glucose levels were investigated in rats. p-Chloroamphetamine elicited a significant hyperglycemia. The hyperglycemic effects of p-chloroamphetamine were completely prevented by the 5-HT synthesis inhibitor, p-chlorophenylalanine. Prior adrenodemedullation abolished the hyperglycemia elicited by p-chloroamphetamine. p-Chloroamphetamine-induced hyperglycemia was prevented by methysergide, which blocks the 5-HT1 and 5-HT2 receptor, the 5-HT1A/1B/2C receptor antagonist, (-)-propranolol, the selective 5-HT1A receptor antagonist, 4-(2'-methoxyphenyl-1-[2'-n-2"pyridinyl)-p-iodobenzamido]-ethyl-pi perazine (p-MPPI), the 5-HT2A/2B/2C receptor antagonists, ritanserin and 4-isopropyl-7-methyl-9-(2-hydroxy-1-methyl-propoxycarbonyl)-4,6A,7 ,8,9,10,10A-octahydro-indolo[4,3-FG]quinolone maleate(LY 53857). However, the 5-HT3 and 5-HT4 receptor antagonist, tropisetron, the 5-HT4 receptor antagonist, 2-methoxy-4-amino-5-chloro-benzoic acid 2-(diethylamino) ethyl ester (SDZ 205-557), and the 5-HT2A receptor antagonist, ketanserin, did not affect the p-chloroamphetamine-induced hyperglycemia. These results suggest that p-chloroamphetamine-induced hyperglycemia is elicited by an enhanced 5-HT release and facilitated adrenaline release. Moreover, our results indicate that p-chloroamphetamine-induced hyperglycemia is mediated by 5-HT1A and 5-HT2B/2C receptors.
- Published
- 1998
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