Properties of Ca 2+ oscillations in rat carotid body chemoreceptor cells

Hypoxia elevates intracellular Ca 2+ concentration ([Ca 2+ ]) in carotid body (CB) Type 1 (glomus) cells and thereby stimulates the secretory activity. To understand Ca 2+ signaling mechanisms in more detail, we examined the effects of a wide range of pO 2 on [Ca 2+ ]. Basal level of Ca 2+ oscillations were observed in normoxia. The frequency of Ca 2+ oscillations was highly dependent on perfusion temperature. At 37°C, >60% of cells showed spontaneous Ca 2+ oscillations. The mean frequency of Ca 2+ oscillations in O 2 ‐sensitive cells was ~0.5 per min. Severe hypoxia and anoxia (<20 mmHg) usually elicited a sustained elevation of [Ca 2+ ]. Mild and moderate levels of hypoxia (20–50 mmHg) caused an increase in the frequency of Ca 2+ oscillations by ~20% and ~60%, respectively. Ca 2+ oscillations were inhibited by 0.1 mM 2‐APB (an inhibitor of IP 3 receptor and store‐operated Ca 2+ entry), as well as by removal of extracellular Ca 2+ . Secretory activity was also blocked by 2‐APB and removal of extracellular Ca 2+ . Block of voltage‐dependent K+ channels with 3 mM TEA enhanced hypoxia‐induced increase in Ca 2+ oscillations by ~20%, indicating that Kv helps limit the Ca 2+ response to mild and moderate hypoxia. Our results show that an increase Ca 2+ oscillations, rather than a sustained rise in [Ca 2+ ], underlies the stimulatory effects of mild and moderate levels of hypoxia on glomus cell activity. Support or Funding Information Supported by NIHCa 2+ oscillationsThis abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal .