Cholecystokinin Induces Cerebral Vasodilatation via Presynaptic CCK 2 Receptors: New Implications for the Pathophysiology of Panic

The authors report that cholecystokinin (CCK), via its subtype 2 receptor (CCK 2 R) 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 smo...

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Published in:Journal of cerebral blood flow and metabolism 2003-03, Vol.23 (3), p.364-370
Main Authors: Sánchez–Fernández, Cristina, González, Carmen, Mercer, Linda D., Beart, Philip M., Ruiz–Gayo, Mariano, Fernández-Alfonso, María S.
Format: Article
Language:English
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Summary:The authors report that cholecystokinin (CCK), via its subtype 2 receptor (CCK 2 R) 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 CCK 2 R antagonist, L-365,260, and antagonized by neuronal NO synthase (nNOS) inhibitors, but was independent of the endothelium. In whole-mount arteries, CCK 2 Rs 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.
ISSN:0271-678X
1559-7016
DOI:10.1097/01.WCB.0000043948.67811.8F