RT info:eu-repo/semantics/article
T1 Carotid body function and ventilatory responses in intermittent hypoxia. evidence for anomalous brainstem integration of arterial chemoreceptor input
A1 Gonzalez‐Martín, M.C.
A1 Vega‐Agapito, M.V.
A1 Conde, Silvia V.
A1 Castañeda, J.
A1 Bustamante, R.
A1 Olea Fraile, Elena
A1 Perez‐Vizcaino, F.
A1 Gonzalez, C.
A1 Obeso, A.
AB Obstructive sleep apnea is a frequent medical condition consisting in repetitive sleep-related episodes of upper airways obstruction andconcurrent events of arterial blood hypoxia. There is a frequent association of cardiovascular diseases and other pathologies to thiscondition conforming the obstructive sleep apnea syndrome (OSAS). Laboratory models of OSAS consist in animals exposed to repetitiveepisodes of intermittent hypoxia (IH) which also develop cardiovascular pathologies, mostly hypertension. The overall OSASpathophysiology appears to be linked to the repetitive hypoxia, which would cause a sensitization of carotid body (CB) chemoreflex andchemoreflex-driven hyperreactivity of the sympathetic nervous system. However, this proposal is uncertain because hyperventilation,reflecting the CB sensitization, and increased plasmaCAlevels, reflecting sympathetic hyperreactivity, are not constant findings in patientswith OSAS and IH animals. Aiming to solve these uncertainties we have studied the entire CB chemoreflex arch in a rat model of IH,including activity of chemoreceptor cells and CB generated afferent activity to brainstem. The efferent activity was measured as ventilationin normoxia, hypoxia, and hypercapnia. Norepinephrine turnover in renal artery sympathetic endings was also assessed. Findings indicate asensitization of the CB function to hypoxia evidenced by exaggerated chemoreceptor cell and CB afferent activity. Yet, IH rats exhibitedmarked hypoventilation in all studied conditions and increased turnover of norepinephrine in sympathetic endings. We conclude that IHproduces a bias in the integration of the input arising from the CB with a diminished drive of ventilation and an exaggerated activation ofbrainstem sympathetic neurons.
PB Elsevier
SN 0021-9541
YR 2011
FD 2011
LK https://uvadoc.uva.es/handle/10324/65861
UL https://uvadoc.uva.es/handle/10324/65861
LA spa
NO Journal of Cellular Physiology, vol 226, n. 8, p1964-1969
NO Producción Científica
DS UVaDOC
RD 26-nov-2024