Sugimoto Y, Yamada J
Department of Pharmacology, Kobe Pharmaceutical University, Japan.
Biol Pharm Bull. 2000 Dec;23(12):1521-3. doi: 10.1248/bpb.23.1521.
Effects of the 5-hydroxytryptamine (5-HT)2A receptor agonist 1-(2,5-dimethoxy-4-iodophenyl)-2-aminopropane (DOI) on plasma glucagon levels were studied in rats. Systemic injection of DOI induces significant increases in plasma glucagon levels. Hyperglucagonemia induced by DOI was dose-dependently prevented by the 5-HT2A receptor antagonist ketanserin. Adrenodemedullation abolished hyperglucagonemia elicited by DOI. Previous report demonstrated that the peripheral 5-HT2A receptor agonist induces hyperglycemia in rats but does not increase plasma glucagon levels at doses inducing hyperglycemia. Therefore, our findings suggest that DOI-induced glucagon release was elicited by stimulation of the central 5-HT2A receptor, which in turn increasing adrenaline release.
在大鼠中研究了5-羟色胺(5-HT)2A受体激动剂1-(2,5-二甲氧基-4-碘苯基)-2-氨基丙烷(DOI)对血浆胰高血糖素水平的影响。全身注射DOI可导致血浆胰高血糖素水平显著升高。5-HT2A受体拮抗剂酮色林可剂量依赖性地阻止DOI诱导的高胰高血糖素血症。肾上腺髓质切除术消除了DOI引起的高胰高血糖素血症。先前的报告表明,外周5-HT2A受体激动剂可诱导大鼠高血糖,但在诱导高血糖的剂量下不会增加血浆胰高血糖素水平。因此,我们的研究结果表明,DOI诱导的胰高血糖素释放是由中枢5-HT2A受体的刺激引起的,进而增加了肾上腺素的释放。