Respiratory physiology & neurobiology

Voltage- and receptor-mediated activation of a non-selective cation channel in rat carotid body glomus cells.

PMID 28013061


A recent study showed that hypoxia activates a Ca(2+)-sensitive, Na(+)-permeable non-selective cation channel (NSC) in carotid body glomus cells. We studied the effects of mitochondrial inhibitors that increase Ca(2+) influx via Ca(2+) channel (Cav), and receptor agonists that release Ca(2+) from endoplasmic reticulum (ER) on NSC. Mitochondrial inhibitors (NaCN, FCCP, H2S, NO) elevated [Ca(2+)]i and activated NSC. Angiotensin II and acetylcholine that elevate [Ca(2+)]i via the Gq-IP3 pathway activated NSC. However, endothelin-1 (Gq) and 5-HT (Gq) showed little or no effect on [Ca(2+)]i and did not activate NSC. Adenosine (Gs) caused a weak rise in [Ca(2+)]i but did not activate NSC. Dopamine (Gs) and γ-aminobytyric acid (Gi) were ineffective in raising [Ca(2+)]i and failed to activate NSC. Store-operated Ca(2+) entry (SOCE) produced by depletion of Ca(2+) stores with cyclopiazonic acid activated NSC. Our results show that Ca(2+) entry via Cav, ER Ca(2+) release and SOCE can activate NSC. Thus, NSC contributes to both voltage- and receptor-mediated excitation of glomus cells.