Oxygen sensing by the carotid body chemoreceptors

Carotid bodies are sensory organs that detect changes in arterial blood oxy gen, and the ensuing reflexes are critical for maintaining homeostasis duri ng hypoxemia. During the past decade, tremendous progress has been made tow ard understanding the cellular mechanisms underlying oxygen sensing at the carotid body. The purpose of this minireview is to highlight some recent co ncepts on sensory transduction and transmission at the carotid body. A bulk of evidence suggests that glomus (type I) cells are the initial site of tr ansduction and that they release transmitters in response to hypoxia, which causes depolarization of nearby afferent nerve endings, leading to an incr ease in sensory discharge. There are two main hypotheses to explain the tra nsduction process that triggers transmitter release. One hypothesis assumes that a biochemical event associated with a heme protein triggers the trans duction cascade. The other hypothesis suggests that a K+ channel protein is the oxygen sensor and that inhibition of this channel by hypoxia leading t o depolarization is a seminal event in transduction. Although there is body of evidence supporting and questioning each of these, this review will try to point out that the truth lies somewhere in an interrelation between the two. Several transmitters have been identified in glomus cells, and they a re released in response to hypoxia. However, their precise roles in sensory transmission remain uncertain. It is hoped that future studies involving t ransgenic animals with targeted disruption of genes encoding transmitters a nd their receptors may resolve some of the key issues surrounding the senso ry transmission at the carotid body. Further studies are necessary to ident ify whether a single sensor or multiple oxygen sensors are needed for the t ransduction process.