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Am J Physiol Endocrinol Metab (April 30, 2002). doi:10.1152/ajpendo.00044.2002
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Articles in PresS, published online ahead of print April 30, 2002
Am J Physiol Endocrinol Metab, 10.1152/ajpendo.00044.2002
Submitted on February 1, 2002
Accepted on April 25, 2002

GLUCOSE-INDUCED ISLET BLOOD FLOW INCREASE IN RATS: AN INTERACTION BETWEEN NERVOUS AND METABOLIC MEDIATORS

Per-Ola Carlsson1*, Richard Olsson1, Orjan Kallskog1, Birgitta Bodin1, Arne Andersson1, and Leif Jansson1

1 Department of Medical Cell Biology, Uppsala University, Uppsala, Sweden

* To whom correspondence should be addressed. E-mail: Per-Ola.Carlsson{at}medcellbiol.uu.se.

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 observed 3, 10 and 20 min after injection of glucose, whereas theophylline (a non-specific adenosine receptor antagonist) prevented the islet blood flow increase 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, whilst the increase in islet blood perfusion seen at 10 and 20 min after glucose administration is caused by both the vagal nerve and adenosine.




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