Obstructive sleep apnea is a frequent medical condition consisting in repetitive sleep-related episodes of upper airways obstruction and
concurrent events of arterial blood hypoxia. There is a frequent association of cardiovascular diseases and other pathologies to this
condition conforming the obstructive sleep apnea syndrome (OSAS). Laboratory models of OSAS consist in animals exposed to repetitive
episodes of intermittent hypoxia (IH) which also develop cardiovascular pathologies, mostly hypertension. The overall OSAS
pathophysiology appears to be linked to the repetitive hypoxia, which would cause a sensitization of carotid body (CB) chemoreflex and
chemoreflex-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 patients
with 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 ventilation
in normoxia, hypoxia, and hypercapnia. Norepinephrine turnover in renal artery sympathetic endings was also assessed. Findings indicate a
sensitization of the CB function to hypoxia evidenced by exaggerated chemoreceptor cell and CB afferent activity. Yet, IH rats exhibited
marked hypoventilation in all studied conditions and increased turnover of norepinephrine in sympathetic endings. We conclude that IH
produces a bias in the integration of the input arising from the CB with a diminished drive of ventilation and an exaggerated activation of
brainstem sympathetic neurons.
