ArticlePloS one2012
Hydrogen sulfide inhibits L-type calcium currents depending upon the protein sulfhydryl state in rat cardiomyocytes.
Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
36 citing papers in PubMed, 70 citations in OpenAlex.
- Black gas, bright future: HNeurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2025Review
- Hydrogen sulfide responsive nanoplatforms: Novel gas responsive drug delivery carriers for biomedical applications.Asian journal of pharmaceutical sciences · 2024Review
- Hydrogen sulfide-induced post-translational modification as a potential drug target.Genes & diseases · 2023Review
- A case of syncope in a villager with hypertrophic cardiomyopathy after hydrogen sulfide exposure by an unauthorized discharge of wastewater.Annals of occupational and environmental medicine · 2023Article
- T-type calcium channel modulation by hydrogen sulfide in neuropathic pain conditions.Frontiers in pharmacology · 2023Review
- Neuroprotective Effects of Early Brain Injury after Subarachnoid Hemorrhage in Rats by Calcium Channel Mediating Hydrogen Sulfide.Cellular and molecular neurobiology · 2021Article
- Hydrogen Sulfide and its Interaction with Other Players in Inflammation.Advances in experimental medicine and biology · 2021Article
- Air Pollution and Cardiac Arrhythmias: From Epidemiological and Clinical Evidences to Cellular Electrophysiological Mechanisms.Frontiers in cardiovascular medicine · 2021Review
- Interaction among Hydrogen Sulfide and Other Gasotransmitters in Mammalian Physiology and Pathophysiology.Advances in experimental medicine and biology · 2021Review
- Hydrogen Sulfide-Evoked Intracellular CaCancers · 2020Article
- Inflammation and its resolution in atherosclerosis: mediators and therapeutic opportunities.Nature reviews. Cardiology · 2019Review
- Pro-arrhythmic Effects of Hydrogen Sulfide in Healthy and Ischemic Cardiac Tissues: Insight From a Simulation Study.Frontiers in physiology · 2019Article
- Methylene Blue Counteracts HCardiovascular toxicology · 2018Article
- Sulfur-containing gaseous signal molecules, ion channels and cardiovascular diseases.British journal of pharmacology · 2018Review
- Protein S-sulfhydration by hydrogen sulfide in cardiovascular system.British journal of pharmacology · 2018Review
- The dichotomous role of HBiochemical pharmacology · 2018Review
- Hydrogen sulfide attenuates isoflurane-induced neuroapoptosis and cognitive impairment in the developing rat brain.BMC anesthesiology · 2017Article
- Vascular biology of hydrogen sulfide.American journal of physiology. Cell physiology · 2017Review
- H2S concentrations in the heart after acute H2S administration: methodological and physiological considerations.American journal of physiology. Heart and circulatory physiology · 2016Article
- 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
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Hydrogen sulfide (H(2)S) is a novel gasotransmitter that inhibits L-type calcium currents (I (Ca, L)). However, the underlying molecular mechanisms are unclear. In particular, the targeting site in the L-type calcium channel where H(2)S functions remains unknown. The study was designed to investigate if the sulfhydryl group could be the possible targeting site in the L-type calcium channel in rat cardiomyocytes. Cardiac function was measured in isolated perfused rat hearts. The L-type calcium currents were recorded by using a whole cell voltage clamp technique on the isolated cardiomyocytes. The L-type calcium channel containing free sulfhydryl groups in H9C2 cells were measured by using Western blot. The results showed that sodium hydrosulfide (NaHS, an H(2)S donor) produced a negative inotropic effect on cardiac function, which could be partly inhibited by the oxidant sulfhydryl modifier diamide (DM). H(2)S donor inhibited the peak amplitude of I( Ca, L) in a concentration-dependent manner. However, dithiothreitol (DTT), a reducing sulfhydryl modifier markedly reversed the H(2)S donor-induced inhibition of I (Ca, L) in cardiomyocytes. In contrast, in the presence of DM, H(2)S donor could not alter cardiac function and L type calcium currents. After the isolated rat heart or the cardiomyocytes were treated with DTT, NaHS could markedly alter cardiac function and L-type calcium currents in cardiomyocytes. Furthermore, NaHS could decrease the functional free sulfhydryl group in the L-type Ca(2+) channel, which could be reversed by thiol reductant, either DTT or reduced glutathione. Therefore, our results suggest that H(2)S might inhibit L-type calcium currents depending on the sulfhydryl group in rat cardiomyocytes.
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