Oxygen sensing is a fundamental biological process necessary for the adaptation of living organisms to variable habitats and physiologic situations. In mammals, acute hypoxia triggers fast respiratory and cardiovascular counter-regulatory adjustments to ensure sufficient 02 supply to the most critical organs such as the brain or the heart. Reduction of blood 02 tension (Po2) is sensed by the arterial chemoreceptors, which generate afferent chemosensory discharges that activate the brain to evoke hyperventilation and sympathetic activation (for a review see Ref. 22). The main arterial chemoreceptor is the carotid body, a minute bilateral organ located in the bifurcation of the carotid artery which contains neurosecretory glomus, or type I, cells and the less numerous substentacular, or type II, cells. Glomus cells, the 02-sensitive elements in the carotid body, are electrically excitable (9, 20) and have 02-sensitive potassium channels in their membranes (3, 7, 20, 33, 36). It is broadly accepted that inhibition of these channels by low Po2 is a major 02-dependent event leading to membrane depolarization, external calcium influx and activation of neurotransmitter release, which, in turn, stimulates the afferent sensory fibers. This model of chemotransduction, suggested by the electrophysiological experiments, has been confirmed in single Fura 2-loaded cells by monitoring cytosolic [Ca2+] and quantal catecholamine secretion (4, 5, 21, 26, 30, 39).
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