RT info:eu-repo/semantics/article
T1 Pulmonary vascular responses to chronic intermittent hypoxia in a guinea pig model of obstructive sleep apnea
A1 Olea Fraile, Elena
A1 Valverde Pérez, Esther
A1 Docio Cuadrado, Inmaculada
A1 Prieto Lloret, Jesús
A1 Aaronson, Philip Irving
A1 Rocher Martín, María Asunción
K1 Pulmonary hypertension
K1 Hipertensión pulmonar
K1 Hipertensión arterial
K1 Hypoxia
K1 Anoxemia
K1 Respiratory organs -Diseases
K1 Organos respiratorios - Enfermedades
K1 Lungs - Blood-vessels - Diseases
K1 Pulmones - Vasos sanguíneos - Enfermedades
K1 Carotid body
K1 Cuerpo carotídeo
K1 Autonomic nervous system
K1 Nervioso Autónomo, Sistema
K1 Sleep apnea syndromes
K1 Síndrome de la apnea del sueño
K1 Endothelial function
K1 Endotelio vascular
K1 Guinea pig
K1 Animales de laboratorio
K1 Medicine
K1 3205.08 Enfermedades Pulmonares
K1 32 Ciencias Médicas
AB Experimental evidence suggests that chronic intermittent hypoxia (CIH), a major hallmark of obstructive sleep apnea (OSA), boosts carotid body (CB) responsiveness, thereby causing increased sympathetic activity, arterial and pulmonary hypertension, and cardiovascular disease. An enhanced circulatory chemoreflex, oxidative stress, and NO signaling appear to play important roles in these responses to CIH in rodents. Since the guinea pig has a hypofunctional CB (i.e., it is a natural CB knockout), in this study we used it as a model to investigate the CB dependence of the effects of CIH on pulmonary vascular responses, including those mediated by NO, by comparing them with those previously described in the rat. We have analyzed pulmonary artery pressure (PAP), the hypoxic pulmonary vasoconstriction (HPV) response, endothelial function both in vivo and in vitro, and vascular remodeling (intima–media thickness, collagen fiber content, and vessel lumen area). We demonstrate that 30 days of the exposure of guinea pigs to CIH (FiO2, 5% for 40 s, 30 cycles/h) induces pulmonary artery remodeling but does not alter endothelial function or the contractile response to phenylephrine (PE) in these arteries. In contrast, CIH exposure increased the systemic arterial pressure and enhanced the contractile response to PE while decreasing endothelium-dependent vasorelaxation to carbachol in the aorta without causing its remodeling. We conclude that since all of these effects are independent of CB sensitization, there must be other oxygen sensors, beyond the CB, with the capacity to alter the autonomic control of the heart and vascular function and structure in CIH.
PB MDPI
SN 1422-0067
YR 2024
FD 2024
LK https://uvadoc.uva.es/handle/10324/70072
UL https://uvadoc.uva.es/handle/10324/70072
LA eng
NO International Journal of Molecular Sciences, 2024, Vol. 25, Nº. 13, 7484
NO Producción Científica
DS UVaDOC
RD 24-nov-2024