Glucose-induced intestinal vasodilation via adenosine A1 receptors requires nitric oxide but not K(+)(ATP) channels.

@article{Matheson2011GlucoseinducedIV,
  title={Glucose-induced intestinal vasodilation via adenosine A1 receptors requires nitric oxide but not K(+)(ATP) channels.},
  author={Paul J. Matheson and Na Li and Patrick D. Harris and El Rasheid Zakaria and Richard Neal Garrison},
  journal={The Journal of surgical research},
  year={2011},
  volume={168 2},
  pages={
          179-87
        }
}
BACKGROUND Both nitric oxide (NO) and adenosine A1 receptor activation mediate microvascular vasodilation during intestinal glucose absorption. Our overall hypothesis is that adenosine triphosphate (ATP) utilization during glucose absorption would increase adenosine metabolite release, which acts on adenosine A1 receptors to alter endothelial production of NO and/or activate ATP-dependent potassium channels (K(+)(ATP)) to dilate intestinal microvessels. METHODS Intravital videomicroscopy of… CONTINUE READING

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