Chronic intermittent hypoxia-induced vascular enlargement and VEGF upregulation in the rat carotid body is not prevented by antioxidant treatment

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dc.contributor.authorDel Rio, Rodrigo
dc.contributor.authorMunoz, Cristian
dc.contributor.authorArias, Paulina
dc.contributor.authorCourt, Felipe A.
dc.contributor.authorMoya, Esteban A.
dc.contributor.authorIturriaga, Rodrigo
dc.date.accessioned2025-01-21T00:00:25Z
dc.date.available2025-01-21T00:00:25Z
dc.date.issued2011
dc.description.abstractDel Rio R, Munoz C, Arias P, Court FA, Moya EA, Iturriaga R. Chronic intermittent hypoxia-induced vascular enlargement and VEGF upregulation in the rat carotid body is not prevented by antioxidant treatment. Am J Physiol Lung Cell Mol Physiol 301: L702-L711, 2011. First published August 5, 2011; doi:10.1152/ajplung.00128.2011.-Chronic intermittent hypoxia (CIH), a characteristic of sleep obstructive apnea, enhances carotid body (CB) chemosensory responses to hypoxia, but its consequences on CB vascular area and VEGF expression are unknown. Accordingly, we studied the effect of CIH on CB volume, glomus cell numbers, blood vessel diameter and number, and VEGF immunoreactivity (VEGF-ir) in male Sprague-Dawley rats exposed to 5% O-2, 12 times/h for 8 h or sham condition for 21 days. We found that CIH did not modify the CB volume or the number of glomus cells but increased VEGF-ir and enlarged the vascular area by increasing the size of the blood vessels, whereas the number of the vessels was unchanged. Because oxidative stress plays an essential role in the CIH-induced carotid chemosensory potentiation, we tested whether antioxidant treatment with ascorbic acid may impede the vascular enlargement and the VEGF upregulation. Ascorbic acid, which prevents the CB chemosensory potentiation, failed to impede the vascular enlargement and the increased VEGF-ir. Thus present results suggest that the CB vascular enlargement induced by CIH is a direct effect of intermittent hypoxia and not secondary to the oxidative stress. Accordingly, the subsequent capillary changes may be secondary to the mechanisms involved in the neural chemosensory plasticity induced by intermittent hypoxia.
dc.fuente.origenWOS
dc.identifier.doi10.1152/ajplung.00128.2011
dc.identifier.eissn1522-1504
dc.identifier.issn1040-0605
dc.identifier.urihttps://doi.org/10.1152/ajplung.00128.2011
dc.identifier.urihttps://repositorio.uc.cl/handle/11534/95340
dc.identifier.wosidWOS:000298158100009
dc.issue.numero5
dc.language.isoen
dc.pagina.finalL711
dc.pagina.inicioL702
dc.revistaAmerican journal of physiology-lung cellular and molecular physiology
dc.rightsacceso restringido
dc.subjectblood vessels
dc.subjectoxidative stress
dc.subject.ods03 Good Health and Well-being
dc.subject.odspa03 Salud y bienestar
dc.titleChronic intermittent hypoxia-induced vascular enlargement and VEGF upregulation in the rat carotid body is not prevented by antioxidant treatment
dc.typeartículo
dc.volumen301
sipa.indexWOS
sipa.trazabilidadWOS;2025-01-12
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