CGRP signalling inhibits NO production through pannexin-1 channel activation in endothelial cells

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dc.contributor.authorGaete, Pablo S.
dc.contributor.authorLillo, Mauricio A.
dc.contributor.authorPuebla, Mariela
dc.contributor.authorPoblete, Ines
dc.contributor.authorFigueroa, Xavier F.
dc.date.accessioned2025-01-23T21:14:00Z
dc.date.available2025-01-23T21:14:00Z
dc.date.issued2019
dc.description.abstractBlood flow distribution relies on precise coordinated control of vasomotor tone of resistance arteries by complex signalling interactions between perivascular nerves and endothelial cells. Sympathetic nerves are vasoconstrictors, whereas endothelium-dependent NO production provides a vasodilator component. In addition, resistance vessels are also innervated by sensory nerves, which are activated during inflammation and cause vasodilation by the release of calcitonin gene-related peptide (CGRP). Inflammation leads to superoxide anion (O-2(center dot-)) formation and endothelial dysfunction, but the involvement of CGRP in this process has not been evaluated. Here we show a novel mechanistic relation between perivascular sensory nerve-derived CGRP and the development of endothelial dysfunction. CGRP receptor stimulation leads to pannexin-1-formed channel opening and the subsequent O-2(center dot-)-dependent connexin-based hemichannel activation in endothelial cells. The prolonged opening of these channels results in a progressive inhibition of NO production. These findings provide new therapeutic targets for the treatment of the inflammation-initiated endothelial dysfunction.
dc.fuente.origenWOS
dc.identifier.doi10.1038/s41598-019-44333-w
dc.identifier.issn2045-2322
dc.identifier.urihttps://doi.org/10.1038/s41598-019-44333-w
dc.identifier.urihttps://repositorio.uc.cl/handle/11534/101013
dc.identifier.wosidWOS:000469217100008
dc.language.isoen
dc.revistaScientific reports
dc.rightsacceso restringido
dc.subject.ods03 Good Health and Well-being
dc.subject.odspa03 Salud y bienestar
dc.titleCGRP signalling inhibits NO production through pannexin-1 channel activation in endothelial cells
dc.typeartículo
dc.volumen9
sipa.indexWOS
sipa.trazabilidadWOS;2025-01-12
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