Diabetes and Impaired Response of Glucagon Cells and Vascular Bed to Adenosine in Rat Pancreas

  1. Marie-Madeleine Loubatieres-Mariani
  1. Faculty of Medicine, Pharmacology Laboratory, Unité de Recherche Associeé 599 du Centre National de la Recherche Scientifique Montpellier, France
  1. Address correspondence and reprint requests to Professor M.-M. Loubatieres, Faculté de Médecine, Laboratoire de Pharmacologie, Institut de Biologie, Boulevard Henri IV, 34060 Montpellier Cedex, France.


Previous studies have shown that adenosine, by activation of purinergic A2-receptors, stimulates glucagon secretion and increases vascular flow rate in isolated perfused pancreases from nondiabetic rats. Because α-cell function and blood flow control are known to be disturbed in diabetes, we investigated whether adenosine was still effective in streptozocininduced diabetic (STZ-D) rats. Our experiments were performed on isolated perfused rat pancreases. Whereas, in normal rats, adenosine (1.65 μM) induced a 200% increase in glucagon output and a 25% rise in the pancreatic vascular flow rate, in rats diabetic for 5–6 wk, this nucleoside was ineffective on glucagon secretion, and its vasodilatory effect was strongly reduced. Long-term in vivo insulin treatment that reversed high glycemia levels was able to restore in large part both adenosine effects. In contrast, a shortterm in vitro pretreatment with insulin was unable to restore the nucleoside effects. We conclude that STZ-D suppresses the stimulatory effect of adenosine on α-cells and strongly reduces its vasodilator properties; these abnormalities may be corrected in large part by long-term insulin treatment with normalization of glycemia.

  • Received December 29, 1988.
  • Revision received June 7, 1989.
  • Accepted June 7, 1989.
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