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The aortic body chemoreceptor is a small cluster of peripheral chemosensory cells located in the arch of the aorta that monitors changes in arterial blood chemistry, specifically oxygen tension (PaO2), carbon dioxide tension (PaCO2), and pH [4, 7]. It consists of type I (glomus) cells, which act as the primary sensory transducers, and type II (sustentacular) cells that provide structural and metabolic support [3, 14]. When hypoxia, hypercapnia, or acidosis is detected, glomus cells depolarize and release excitatory neurotransmitters that stimulate the vagus nerve (cranial nerve X), which transmits signals to the medullary respiratory and vasomotor centers [10, 15]. Although the carotid bodies are the primary drivers of the human ventilatory response to hypoxia, the aortic body plays a significant role in cardiovascular homeostasis and is notably sensitive to changes in total blood oxygen content, such as during carbon monoxide poisoning or anemia [4, 16]. Pathological overactivity of these chemoreceptors has been linked to the development of sympathetic-mediated conditions like hypertension and heart failure, making the ion channels and receptors within these bodies potential targets for drug development [11, 13].
Drugs modulate the aortic body primarily by acting on the molecular components of glomus cells, such as inhibiting oxygen-sensitive potassium channels (TASK-1, BK channels) or activating/blocking neurotransmitter receptors (P2X3, D2, or nicotinic receptors), which in turn alters the rate of action potential transmission via the vagus nerve to the medulla [3, 11, 14].
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