title: Voltage- and receptor-mediated activation of a non-selective cation channel in rat carotid body glomus cells.
abstract: A recent study showed that hypoxia activates a Ca2+-sensitive, Na+-permeable non-selective cation channel (NSC) in carotid body glomus cells. We studied the effects of mitochondrial inhibitors that increase Ca2+influx via Ca2+channel (Cav), and receptor agonists that release Ca2+from endoplasmic reticulum (ER) on NSC. Mitochondrial inhibitors (NaCN, FCCP, H2S, NO) elevated [Ca2+]iand activated NSC. Angiotensin II and acetylcholine that elevate [Ca2+]ivia the Gq-IP3pathway activated NSC. However, endothelin-1 (Gq) and 5-HT (Gq) showed little or no effect on [Ca2+]iand did not activate NSC. Adenosine (Gs) caused a weak rise in [Ca2+]ibut did not activate NSC. Dopamine (Gs) and γ-aminobytyric acid (Gi) were ineffective in raising [Ca2+]iand failed to activate NSC. Store-operated Ca2+entry (SOCE) produced by depletion of Ca2+stores with cyclopiazonic acid activated NSC. Our results show that Ca2+entry via Cav, ER Ca2+release and SOCE can activate NSC. Thus, NSC contributes to both voltage- and receptor-mediated excitation of glomus cells.
authors.affiliation: Department of Physiology and Biophysics, Chicago Medical School, Rosalind Franklin University of Medicine and Science, 3333 Green Bay Road, North Chicago, IL 60064, USA.
authors.forename: Jiaju
authors.initials: J
authors.lastname: Wang
authors.affiliation: Department of Physiology and Biophysics, Chicago Medical School, Rosalind Franklin University of Medicine and Science, 3333 Green Bay Road, North Chicago, IL 60064, USA.
authors.forename: James O
authors.initials: JO
authors.lastname: Hogan
authors.affiliation: Department of Physiology and Biophysics, Chicago Medical School, Rosalind Franklin University of Medicine and Science, 3333 Green Bay Road, North Chicago, IL 60064, USA. Electronic address: donghee.kim@rosalindfranklin.edu.
authors.forename: Donghee
authors.initials: D
authors.lastname: Kim
mesh_terms: D000200:Action Potentials / Q000187:drug effects / Q000502:physiology; D000804:Angiotensin II / Q000494:pharmacology; D000813:Anilides / Q000494:pharmacology; D000818:Animals; D000831:Animals, Newborn; D002110:Caffeine / Q000494:pharmacology; D002118:Calcium / Q000378:metabolism* / Q000494:pharmacology; D002121:Calcium Channel Blockers / Q000494:pharmacology; D002259:Carbonyl Cyanide p-Trifluoromethoxyphenylhydrazone / Q000494:pharmacology; D002344:Carotid Body / Q000166:cytology*; D002628:Chemoreceptor Cells / Q000187:drug effects / Q000502:physiology*; D004305:Dose-Response Relationship, Drug; D004721:Endoplasmic Reticulum / Q000187:drug effects / Q000378:metabolism; D004791:Enzyme Inhibitors / Q000494:pharmacology; D000860:Hypoxia / Q000503:physiopathology; D007473:Ion Channels / Q000378:metabolism*; D061209:Proton Ionophores / Q000494:pharmacology; D051381:Rats; D017207:Rats, Sprague-Dawley; D026423:S-Nitroso-N-Acetylpenicillamine / Q000494:pharmacology; D012966:Sodium Cyanide / Q000494:pharmacology; D013830:Thiadiazoles / Q000494:pharmacology
chemical_list: C476308:4-methyl-4'-(3,5-bis(trifluoromethyl)-1H-pyrazol-1-yl)-1,2,3-thiadiazole-5-carboxanilide; D000813:Anilides; D002121:Calcium Channel Blockers; D004791:Enzyme Inhibitors; D007473:Ion Channels; D061209:Proton Ionophores; D013830:Thiadiazoles; D000804:Angiotensin II; D002259:Carbonyl Cyanide p-Trifluoromethoxyphenylhydrazone; D002110:Caffeine; D026423:S-Nitroso-N-Acetylpenicillamine; D012966:Sodium Cyanide; D002118:Calcium
keywords: Calcium; Carotid body; G proteins; Hypoxia; Mitochondria; Receptors