Abu-Basha E A, Makowski J P, Yibchok-anun S, Hsu W H
Department of Biomedical Sciences, Iowa State University, Ames 50011-1250, USA.
Metabolism. 2000 Oct;49(10):1370-3. doi: 10.1053/meta.2000.9511.
The purpose of the study is to investigate the direct effect of bradykinin (BK), a potent vasoactive nonapeptide, on glucagon secretion from the perfused rat pancreas. BK (0.1, 1, and 10 micromol/L) increased glucagon secretion in a concentration-dependent manner. HOE 140, a BK2 receptor antagonist (0.01, 0.1, and 1 nmol/L), prevented the stimulatory effect of BK on glucagon secretion in a concentration-dependent manner. In contrast, des-Arg9,Leu8-BK, a BK1 receptor antagonist (1 nmol/L), failed to antagonize the effect of BK. Thus, BK stimulates glucagon secretion from the perfused rat pancreas by activating BK2 receptors, but not BK1 receptors.
本研究的目的是调查缓激肽（一种有效的血管活性九肽）对灌注大鼠胰腺中胰高血糖素分泌的直接影响。缓激肽（0.1、1和10微摩尔/升）以浓度依赖性方式增加胰高血糖素分泌。HOE 140，一种缓激肽2受体拮抗剂（0.01、0.1和1纳摩尔/升），以浓度依赖性方式阻止缓激肽对胰高血糖素分泌的刺激作用。相比之下，des-Arg9,Leu8-缓激肽，一种缓激肽1受体拮抗剂（1纳摩尔/升），未能拮抗缓激肽的作用。因此，缓激肽通过激活缓激肽2受体而非缓激肽1受体来刺激灌注大鼠胰腺中的胰高血糖素分泌。
