Glucose-induced islet blood flow increase in rats:: interaction between nervous and metabolic mediators
Glucose-induced islet blood flow increase in rats:: interaction between nervous and metabolic mediators
复制标题
DOI：
10.1152/ajpendo.00044.2002
复制
发表时间：
2002-09-01
影响因子：
5.1
通讯作者：
Jansson, L
中科院分区：
文献类型：
--
作者：
Carlsson, PO;Olsson, R;Jansson, L
这项研究研究了大鼠葡萄糖诱导的胰岛血流增加的机制。用微球技术评估腺苷，腺苷受体拮抗剂和迷走神经流动对胰岛血流的影响。迷走术防止注射葡萄糖后3、10和20分钟的胰岛流量增加，而茶碱（一种非特异性腺苷受体拮抗剂）阻止了葡萄糖给药后10和20分钟的胰岛流量增加。选择性腺苷受体拮抗剂的给药表明，对茶碱的反应是由A（1）受体介导的。腺苷的外源给药不会影响胰岛的血流，但是腺苷摄取抑制剂二吡啶胺引起的腺苷的局部积累导致胰岛血流增加了一倍。总之，诱导高血糖后3分钟的胰岛血流增加是由迷走神经引起的，而葡萄糖给药后10和20分钟的胰岛血液灌注的增加是由迷走神经和腺苷引起的。
This study investigated the mechanisms for glucose-induced islet blood flow increase in rats. The effects of adenosine, adenosine receptor antagonists, and vagotomy on islet blood flow were evaluated with a microsphere technique. Vagotomy prevented the islet blood flow increase expected 3, 10, and 20 min after injection of glucose, whereas theophylline (a nonspecific adenosine receptor antagonist) prevented the islet blood flow increase from occurring 10 and 20 min after glucose administration. Administration of selective adenosine receptor antagonists suggested that the response to theophylline was mediated by A(1) receptors. Exogenous administration of adenosine did not affect islet blood flow, but local accumulation of adenosine, induced by the adenosine uptake inhibitor dipyridamole, caused a doubling of islet blood flow. In conclusion, the increased islet blood flow seen 3 min after induction of hyperglycemia is caused by the vagal nerve, whereas the increase in islet blood perfusion seen at 10 and 20 min after glucose administration is caused by both the vagal nerve and adenosine.