Glucose-induced insulin secretion and α2-adrenergic receptor subtypes

Hiroshi Hirose, Hiroshi Maruyama, Katsuhiko Ito, Kazunori Koyama, Koichi Kido, Takao Saruta

研究成果: Article査読

21 被引用数 (Scopus)


α2-Adrenoceptor antagonists have been investigated in human in vivo studies as new oral antihyperglycemic agents. α2-Adrenoceptors are subdivided into α2A and α2B subtypes by using receptor-binding methods or cloning methods. This study was designed to determine the α2-adrenergic receptor subtype(s) involved in glucose-induced insulin and glucagon secretion from the isolated perfused rat pancreas at a glucose concentration of 16.7 mmol/L Both the α2A-preferentlal agonist oxymetazoline and the non-subtype-selective α2-agonist p-aminoclonidine, at concentrations above 10-9 mol/L, significantly inhibited glucose-induced insulin secretion (p < 0.05 and p < 0.01, respectively) and stimulated glucagon secretion from 10-7 mol/L, as compared with basal levels (p < 0.01, respectively). In contrast, the α1-selective agonist phenylephrine, at concentrations up to 10-6 mol/L, affected neither insulin nor glucagon secretion as compared with basal levels. Furthermore, the non-subtype-selective α2-antagonist rauwolscine, at concentrations above 10-6 mol/L, and the α2A-preferential antagonist WB-4101, at 10-5 mol/L, significantly antagonized the effects of 10-5 mol/L p-aminoclonidine on both insulin and glucagon secretion (p < 0.01 and p < 0.05, respectively). In contrast, neither the α1- and α2B-selective antagonist prazosin nor the α2B-preferential antagonist chlorpromazine, at concentrations up to 10-5 mol/L, antagonized the effects of p-aminoclonidine. These results suggest that α2A rather than α2B-adrenergic agonism inhibits glucose-induced insulin secretion and stimulates glucagon secretion in the isolated perfused rat pancreas.

ジャーナルThe Journal of Laboratory and Clinical Medicine
出版ステータスPublished - 1993 1月

ASJC Scopus subject areas

  • 病理学および法医学


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