Carotid body chemoreceptors, sympathetic neural activation, and cardiometabolic disease

Abstract

The carotid body (CB) is the main peripheral chemoreceptor that senses the arterial PO2, PCO2 and pH. In response to hypoxemia, hypercapnia and acidosis, carotid chemosensory discharge elicits reflex respiratory, autonomic and cardiovascular adjustments. The classical construct considers the CB as the main peripheral oxygen sensor, triggering reflex physiological responses to acute hypoxemia and facilitating the ventilatory acclimation to chronic hypoxemia at high altitude. However, a growing body of experimental evidence supports the novel concept that an abnormally enhanced CB chemosensory input to the brainstem contributes to overactivation of the sympathetic nervous system, and consequent pathology. Indeed, the CB has been implicated in several diseases associated with increases in central sympathetic outflow. These include hypertension, heart failure, sleep apnea, chronic obstructive pulmonary disease and metabolic syndrome. Indeed, ablation of the CB has been proposed for the treatment of severe and resistant hypertension in humans. In this review, we will analyze and discuss new evidence supporting an important role for the CB chemoreceptor in the progression of autonomic and cardiorespiratory alterations induced by heart failure, obstructive sleep apnea, chronic obstructive pulmonary disease and metabolic syndrome.

Heart Rate Recovery After 6-min Walking Test Predicts Acute Exacerbation in COPD

“…Although the relationship between autonomic cardiac dysfunction and COPD is not fully clarified, our findings provide evidence that chronic complex diseases, such as COPD, are associated with autonomic dysfunction and sympathetic over activation (13). Moreover, a recent published study indicates that heart rate variability (HRV) at rest (as expression of autonomic imbalance) during AECOPD might increase the risk of sudden death (14).…”

Mechanisms in fluid retention – towards a mutual concept

“…Substantial evidence suggests that the negative feedback from low-pressure baroreceptors is blunted in heart failure resulting in increased and sustained activation of the SNS with high circulating noradrenaline concentrations. Other causes have been proposed include sleepbreathing disorders (sleep apnoea), a metaboreflex arising from skeletal muscle adenosine release by angiotensin receptor activation, and prejunctional facilitation of neurotransmission and noradrenaline release at central and peripheral sites (Floras, 2003;Triposkiadis et al, 2009;Costanzo et al, 2015;Iturriaga et al, 2016). Other causes have been proposed include sleepbreathing disorders (sleep apnoea), a metaboreflex arising from skeletal muscle adenosine release by angiotensin receptor activation, and prejunctional facilitation of neurotransmission and noradrenaline release at central and peripheral sites (Floras, 2003;Triposkiadis et al, 2009;Costanzo et al, 2015;Iturriaga et al, 2016).…”

DNA methylation in the central and efferent limbs of the chemoreflex requires carotid body neural activity

“…; Iturriaga et al . ). It was proposed that IH activates the carotid body (CB), which is the major sensory organ for monitoring O 2 levels in the arterial blood and thereby causes reflex activation of the sympathetic nervous system in SA patients (Cistulli & Sullivan, ).…”