Sugimoto Y, Yamada J, Yoshikawa T, Horisaka K
Department of Pharmacology, Kobe Pharmaceutical University, Japan.
Eur J Pharmacol. 1996 Jun 20;307(1):75-80. doi: 10.1016/0014-2999(96)00189-6.
Acute administration of the 5-HT2C/2B receptor agonist 1-(3-chlorophenyl)piperazine (mCPP, 5-10 mg/kg i.p.) induced hyperglycemia in rats. These changes were diminished in a dose-dependent manner by the 5-HT1/5-HT2 receptor antagonist methysergide and the 5-HT2A/2B/2C receptor antagonist ritanserin. In addition, mCPP-induced hyperglycemia was dose dependently diminished by the ganglionic blocker hexamethonium and was prevented by prior adrenodemedullation. Neither the 5-HT2A receptor antagonist ketanserin nor the 5-HT3/5-HT4 receptor antagonist (3-alpha-tropanyl)-1 H-indole-3-carboxylic acid ester (ICS 205-930) proved effective against mCPP-induced hyperglycemia. Lastly, administration of the 5-HT2A/2C receptor agonist 1-(2,5-dimethoxy-4-iodophenyl)2-aminopropane (DOI) increased plasma glucose levels through ketanserin- and ritanserin-sensitive processes. Our results suggest that hyperglycemia elicited by mCPP is mediated by 5-HT2C and/or 2B receptors, and in turn adrenomedullary catecholamine release, whereas that elicited by DOI involves 5-HT2A receptors.
腹腔注射5-羟色胺2C/2B受体激动剂1-(3-氯苯基)哌嗪（mCPP，5-10毫克/千克）可使大鼠急性出现高血糖症。5-羟色胺1/5-羟色胺2受体拮抗剂美西麦角和5-羟色胺2A/2B/2C受体拮抗剂利坦色林可使这些变化呈剂量依赖性减轻。此外，神经节阻断剂六甲铵可使mCPP诱导的高血糖症呈剂量依赖性减轻，而预先进行肾上腺髓质切除可预防该症状。5-羟色胺2A受体拮抗剂酮色林和5-羟色胺3/5-羟色胺4受体拮抗剂（3-α-托烷基）-1H-吲哚-3-羧酸酯（ICS 205-930）均未证明对mCPP诱导的高血糖症有效。最后，5-羟色胺2A/2C受体激动剂1-(2,5-二甲氧基-4-碘苯基)2-氨基丙烷（DOI）通过酮色林和利坦色林敏感的过程提高血浆葡萄糖水平。我们的结果表明，mCPP引发的高血糖症是由5-羟色胺2C和/或2B受体介导的，进而导致肾上腺髓质儿茶酚胺释放，而DOI引发的高血糖症则涉及5-羟色胺2A受体。
