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Am J Physiol Endocrinol Metab 283: E457-E464, 2002. First published April 30, 2002; doi:10.1152/ajpendo.00044.2002
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Vol. 283, Issue 3, E457-E464, September 2002

Glucose-induced islet blood flow increase in rats: interaction between nervous and metabolic mediators

Per-Ola Carlsson, Richard Olsson, Örjan Källskog, Birgitta Bodin, Arne Andersson, and Leif Jansson

Department of Medical Cell Biology, Uppsala University, SE-751 23 Uppsala, Sweden

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 A1 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.

adenosine; microcirculation; microspheres; pancreas; vagus nerve


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