All for one - O2 -sensitive K+ channels that mediate carotid body activation.

Abstract

The hypoxic ventilatory response is a homeostatic reflex essential for the survival of mammals in environmental or pathological conditions that present with hypoxaemia (low urn:x-wiley:00223751:media:tjp12772:tjp12772-math-0001 in the blood ). Changes in blood urn:x-wiley:00223751:media:tjp12772:tjp12772-math-0002 are detected by neural crest -derived and O2-sensitive glomus cells (also named type I or chief cells ) in the carotid body (CB), the most important arterial chemoreceptor organ. In response to hypoxia , CB glomus cells release transmitters to activate afferent sensory fibres that synapse on neurons in the brainstem respiratory centre (for a recent review see López-Barneo et al. 2016). The notion that hypoxia (low urn:x-wiley:00223751:media:tjp12772:tjp12772-math-0003) causes inhibition of membrane K+ conductance in glomus cells to elicit depolarization, voltage-gated Ca2+ entry, and neurotransmitter release is widely accepted; however, the relevance of the several classes of K+ channels expressed in glomus cells for the initiation or maintenance of the hypoxic response is not well understood. In this issue of The Journal of Physiology , Wang & Kim (2018) report an elegant and detailed study suggesting differential roles of background and voltage-dependent K+ channels in hypoxic CB activation.