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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 

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Cholecystokinin induces cerebral vasodilatation via presynaptic CCK2 receptors: new implications for the pathophysiology of panic.

The authors report that cholecystokinin ( CCK), via its subtype 2 receptor (CCK2R) located presynaptically on cerebral arteries, mediates the release of nitric oxide (NO), which induces vasodilatation. Whereas CCK octapeptide and its fragment CCK tetrapeptide (CCK-4) lack a direct effect on the smooth muscle of pial vessels, the authors showed that both CCK peptides modulate the neurogenic responses in bovine cerebral arteries. The neurogenic vasodilatation induced by CCK-4 was blocked by the CCK2R antagonist, L-365,260, and antagonized by neuronal NO synthase (nNOS) inhibitors, but was independent of the endothelium. In whole-mount arteries, CCK2Rs were detected in nerve fibers and colocalized with nNOS and synaptophysin. The findings provide, for the first time, a neural mechanism by which CCK may increase cerebral blood flow.[1]

References

  1. Cholecystokinin induces cerebral vasodilatation via presynaptic CCK2 receptors: new implications for the pathophysiology of panic. Sánchez-Fernández, C., González, C., Mercer, L.D., Beart, P.M., Ruiz-Gayo, M., Fernández-Alfonso, M.S. J. Cereb. Blood Flow Metab. (2003) [Pubmed]
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