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

Autor: Jiaju Wang, James O. Hogan, Donghee Kim
Rok vydání: 2017
Předmět:
Carbonyl Cyanide p-Trifluoromethoxyphenylhydrazone
0301 basic medicine
Physiology
Action Potentials
Endoplasmic Reticulum
Ion Channels
Rats
Sprague-Dawley
chemistry.chemical_compound
Glomus cell
Sodium Cyanide
Anilides
Enzyme Inhibitors
Hypoxia
reproductive and urinary physiology
Carotid Body
Angiotensin II
General Neuroscience
Calcium Channel Blockers
Chemoreceptor Cells
Cell biology
medicine.anatomical_structure
Proton Ionophores
Carotid body
biological phenomena
cell phenomena
and immunity
Cyclopiazonic acid
Acetylcholine
medicine.drug
Pulmonary and Respiratory Medicine
medicine.medical_specialty
S-Nitroso-N-Acetylpenicillamine
Article
03 medical and health sciences
Caffeine
Internal medicine
Thiadiazoles
medicine
Animals
Dose-Response Relationship
Drug
Endoplasmic reticulum
Adenosine
Rats
nervous system diseases
030104 developmental biology
Endocrinology
Animals
Newborn
nervous system
chemistry
Calcium
Carbonyl cyanide-p-trifluoromethoxyphenylhydrazone
Zdroj: Respiratory Physiology & Neurobiology. 237:13-21
ISSN: 1569-9048
DOI: 10.1016/j.resp.2016.12.005
Popis: 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+]i and activated NSC. Angiotensin II and acetylcholine that elevate [Ca2+]i via the Gq-IP3 pathway activated NSC. However, endothelin-1 (Gq) and 5-HT (Gq) showed little or no effect on [Ca2+]i and did not activate NSC. Adenosine (Gs) caused a weak rise in [Ca2+]i but did not activate NSC. Dopamine (Gs) and γ-aminobytyric acid (Gi) were ineffective in raising [Ca2+]i and 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.
Databáze: OpenAIRE
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