Nitric oxide deficit is part of the maladaptive paracrine-autocrine response of the carotid body to intermittent hypoxia in sleep apnea

Abstract

The carotid body functions to maintain the blood gas homeostasis, whereas anomalous carotid chemoreceptor activities could be pathogenic in patients with sleep apnea. Recent findings suggest an upregulation of renin-angiotensin system (Lam SY, Liu Y, Ng KM et al. Exp Physiol 99:220–231, 2014), which could lead to inflammation in the carotid body during intermittent hypoxia (Lam SY, Liu Y, Ng KM et al. Histochem Cell Biol 137:303–317, 2012). In addition, the level of nitric oxide detected in the carotid body was significantly decreased following intermittent hypoxia for days. These locally regulated mechanisms are proposed to be a significant part of the hypoxia-mediated maladaptive changes of the carotid body, which could play a role in the pathophysiological cascade of sleep apnea in patients with an overactivity of the chemoreflex.