ArticlePflugers Archiv : European journal of physiology2012
Effects of exogenous hydrogen sulphide on calcium signalling, background (TASK) K channel activity and mitochondrial function in chemoreceptor cells.
Article in Pflugers Archiv : European journal of physiology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers.
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Who cites it
51 citing papers in PubMed, 97 citations in OpenAlex.
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- Are Multiple Mitochondrial Related Signalling Pathways Involved in Carotid Body Oxygen Sensing?Frontiers in physiology · 2022Review
- Impact of Hydrogen Sulfide on Mitochondrial and Bacterial Bioenergetics.International journal of molecular sciences · 2021Review
- A Case for Hydrogen Sulfide Metabolism as an Oxygen Sensing Mechanism.Antioxidants (Basel, Switzerland) · 2021Review
- Oxygen-dependent regulation of ion channels: acute responses, post-translational modification, and response to chronic hypoxia.Pflugers Archiv : European journal of physiology · 2021Review
- Carotid body chemoreceptors: physiology, pathology, and implications for health and disease.Physiological reviews · 2021Review
- Short-termCell adhesion & migration · 2020Article
- Hydroxycobalamin Reveals the Involvement of Hydrogen Sulfide in the Hypoxic Responses of Rat Carotid Body Chemoreceptor Cells.Antioxidants (Basel, Switzerland) · 2019Article
- HRespiratory physiology & neurobiology · 2019Article
- A1899, PK-THPP, ML365, and Doxapram inhibit endogenous TASK channels and excite calcium signaling in carotid body type-1 cells.Physiological reports · 2018Article
- Acute oxygen sensing by the carotid body: a rattlebag of molecular mechanisms.The Journal of physiology · 2018Review
- Role of reactive oxygen species and sulfide-quinone oxoreductase in hydrogen sulfide-induced contraction of rat pulmonary arteries.American journal of physiology. Lung cellular and molecular physiology · 2018Article
- Recent advances in understanding the physiology of hypoxic sensing by the carotid body.F1000Research · 2018Review
- Is Carotid Body Physiological OFrontiers in physiology · 2018Review
- Voltage- and receptor-mediated activation of a non-selective cation channel in rat carotid body glomus cells.Respiratory physiology & neurobiology · 2017Article
- The emerging role of AMPK in the regulation of breathing and oxygen supply.The Biochemical journal · 2016Review
- Methylene blue counteracts H2S toxicity-induced cardiac depression by restoring L-type Ca channel activity.American journal of physiology. Regulatory, integrative and comparative physiology · 2016Article
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1 author at 1 institution in 1 country.
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Abstract
It has been proposed that endogenous H(2)S mediates oxygen sensing in chemoreceptors; this study investigates the mechanisms by which H(2)S excites carotid body type 1 cells. H(2)S caused a rapid reversible increase in intracellular calcium with EC(50) ≈ 6 μM. This [Ca(2+)](i) response was abolished in Ca-free Tyrode. In perforated patch current clamp recordings, H(2)S depolarised type 1 cells from -59 to -35 mV; this was accompanied by a robust increase in [Ca(2+)](i). Voltage clamping at the resting membrane potential abolished the H(2)S-induced rise in [Ca(2+)](i). H(2)S inhibited background K(+) current in whole cell perforated patch and reduced background K(+) channel activity in cell-attached patch recordings. It is concluded that H(2)S excites type 1 cells through the inhibition of background (TASK) potassium channels leading to membrane depolarisation and voltage-gated Ca(2+) entry. These effects mimic those of hypoxia. H(2)S also inhibited mitochondrial function over a similar concentration range as assessed by NADH autofluorescence and measurement of intracellular magnesium (an index of decline in MgATP). Cyanide inhibited background K channels to a similar extent to H(2)S and prevented H(2)S exerting any further influence over channel activity. These data indicate that the effects of H(2)S on background K channels are a consequence of inhibition of oxidative phosphorylation. Whilst this does not preclude a role for endogenous H(2)S in oxygen sensing via the inhibition of cytochrome oxidase, the levels of H(2)S required raise questions as to the viability of such a mechanism.
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