Abstract
The carotid body is a highly vascularized organ designed to monitor oxygen levels. Reducing oxygen levels in blood results in increased activity of the carotid body cells and reflex increases in sympathetic nerve activity. A key contributor to elevated sympathetic nerve activity in neurogenic forms of hypertension is enhanced peripheral chemoreceptor activity. Hypertension commonly occurs in metabolic disorders, like obesity. Such metabolic diseases are serious global health problems. Yet, the mechanisms contributing to increased sympathetic nerve activity and hypertension in obesity are not fully understood and a better understanding is urgently required. In this review, we examine the literature that suggests that overactivity of the carotid body may also contribute to metabolic disturbances. The purine ATP is an important chemical mediator influencing the activity of the carotid body and the role of purines in the overactivity of the carotid body is explored. We will conclude with the suggestion that tonic overactivity of the carotid body may be a common denominator that contributes to the hypertension and metabolic dysfunction seen in conditions in which metabolic disease exists such as obesity or insulin resistance induced by high caloric intake. Therapeutic treatment targeting the carotid bodies may be a viable treatment since translation to the clinic could be more easily performed than expected via repurposing antagonists of purinergic receptors currently in clinical practice, and the use of other minimally invasive techniques that reduce the overactivity of the carotid bodies which may be developed for such clinical use.
Highlights
The carotid body was primarily regarded as a chemoreceptor organ that regulated oxygen levels in the blood
In patients with newly diagnosed obstructive sleep apnea, augmented cardiovascular and respiratory responses to hypoxia are observed (Narkiewicz et al, 1999). These findings suggest that chronic intermittent hypoxia-induced activation of the chemoreceptor reflex could potentially contribute to pathological cardiovascular and respiratory complications
The adrenal gland showed similar changes in the expression of those enzymes suggesting that increased oxidative stress may occur in the efferent sympathetic outflow and eliciting increased blood pressure. This is supported by the findings that show that scavengers of reactive oxygen species (ROS) can reduce the increased blood pressure elicited by chronic intermittent hypoxia in rodents (Iturriaga et al, 2016), and reduce the overexpression of pro-oxidant enzymes and restores the expression of anti-oxidant enzymes in the glomus cells, brainstem, and adrenal gland suggesting a key link between hyperactive carotid bodies, excessive ROS production and elevated sympathetic nerve activity
Summary
Reducing oxygen levels in blood results in increased activity of the carotid body cells and reflex increases in sympathetic nerve activity. Hypertension commonly occurs in metabolic disorders, like obesity. Such metabolic diseases are serious global health problems. The mechanisms contributing to increased sympathetic nerve activity and hypertension in obesity are not fully understood and a better understanding is urgently required. We examine the literature that suggests that overactivity of the carotid body may contribute to metabolic disturbances. We will conclude with the suggestion that tonic overactivity of the carotid body may be a common denominator that contributes to the hypertension and metabolic dysfunction seen in conditions in which metabolic disease exists such as obesity or insulin resistance induced by high caloric intake.
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