ABSTRACT
Environmental hypoxia evokes a rapid reflex increase in the respiration rate. This reflex is initiated in the carotid bodies located at the bifurcation of the carotid arteries (for review, see Refs. 1-4). Upon a decrease in arterial PO2, the chemoreceptor type I carotid body cells release neurotransmitters that activate afferent sensory fibers of the sinus nerve, stimulating the brainstem respiratory centers and provoking a reflex increase in ventilation. Similarly, neuroepithelial body cells, which are innervated clusters of amine-and peptide-containing cells located within the airway mucosa, are transducers of hypoxic stimuli and function as airway chemoreceptors (for review see Refs. 3 and 4). Besides the release of neurotransmitters and the stimulation of respiration, hypoxia also has a profound adaptive effect on the pulmonary circulation (for review see Refs. 5 and 6). Hypoxia-induced vasoconstriction of resistance pulmonary artery smooth muscle (PASM) leads to a redistribution of the nonoxygenated blood toward better ventilated regions of the lung.
