Saito Y, Kato M, Kubohara Y, Kobayashi I, Tatemoto K
Department of Laboratory Medicine, School of Medicine, Gunma University, Maebashi, Japan.
Biochem Biophys Res Commun. 1996 Apr 25;221(3):577-80. doi: 10.1006/bbrc.1996.0638.
We have examined the effects of bradykinin (BK) on both the intracellular free calcium concentration ([Ca2+]i) and insulin secretion in the hamster beta-cell line, HIT-T15 cells. BK evoked a rise in [Ca2+]i in a dose-dependent manner. This response was suppressed by neomycin, suggesting that BK mobilizes Ca2+ from intracellular store via promotion of the phosphatidyl inositol turnover. Furthermore, BK also evoked insulin secretion. Both the BK-evoked rise in [Ca2+]i and insulin secretion were suppressed by the BK2 receptor antagonist, but not by the BK1 receptor antagonist. These results indicate that BK increases [Ca2+]i via BK2 receptor, thereby promoting insulin secretion in HIT-T15 cells.
我们研究了缓激肽（BK）对仓鼠β细胞系HIT-T15细胞内游离钙浓度（[Ca2+]i）和胰岛素分泌的影响。BK以剂量依赖性方式引起[Ca2+]i升高。新霉素抑制了这种反应，表明BK通过促进磷脂酰肌醇周转从细胞内储存中动员Ca2+。此外，BK还引起胰岛素分泌。BK2受体拮抗剂抑制了BK引起的[Ca2+]i升高和胰岛素分泌，但BK1受体拮抗剂没有。这些结果表明，BK通过BK2受体增加[Ca2+]i，从而促进HIT-T15细胞中的胰岛素分泌。
