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With the exception of anaerobes, organisms depend on oxygen for the production of energy and for biosynthetic reactions. Therefore, cells, tissues, and organisms must be able to sense and respond to changes in the oxygen concentration of their environment. The response of mammalian cells to hypoxia is crucial for their survival, allowing cells to cope with a low-oxygen environment. There are, however, specialized cells located in chemosensory organs (carotid bodies, pulmonary neuroepithelial bodies, and pulmonary artery smooth muscle among others) whose responses to hypoxia are unique, differing both quantitatively and qualitatively from the general self-defense reaction to hypoxia observed in other cell types. The specific hypoxic response of these chemosensitive cells is fast (seconds to minutes), has a lower threshold, requires an increase in their metabolic activity, and leads to changes in their excitability, contractility, and/or secretory activity. All of these features are specializations designed to prevent hypoxia in the entire organism and, thus, to maintain homeostasis.The physiological role of these specialized responses is well characterized, but the molecular mechanisms of O2 sensing and their transduction into an adaptive response in chemoreceptor cells is poorly understood. Over the past decade, it has been well established that modulation of ion channel activity by changes in oxygen levels contributes to the chemoreceptor cell response to low Po2. Since the pioneer description of a low Po2-modulated K+ current in rabbit carotid body chemoreceptor cells1 many other O2-sensitive K+ channels have been identified in chemosensory preparations.2 The high degree of kinetic and pharmacological diversity among O2-sensitive K+ channels has focused our interest toward determining the structural requirements for O2 sensing. Several K+ channel genes expressed in some of the cell types sensitive to hypoxia have …

Are Kv Channels the Essence of O 2 Sensing?

Are Kv Channels the Essence of O ₂ Sensing?