ArticleThe Journal of physiology2013
Hydrogen sulphide inhibits Ca2+ release through InsP3 receptors and relaxes airway smooth muscle.
Article in The Journal of physiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
32 citing papers in PubMed, 54 citations in OpenAlex.
- Hydrogen Sulfide in Balneology: Physiology, Evidence, and Clinical Translation.International journal of molecular sciences · 2025Review
- TMEM16A Antagonism: Therapeutic Potential with Desensitization of β-Agonist Responsiveness in Asthma.American journal of respiratory cell and molecular biology · 2025Article
- The CBS/HCommunications biology · 2024Article
- Article
- Imidazobenzodiazepine PI320 Relaxes Mouse Peripheral Airways by Inhibiting Calcium Mobilization.American journal of respiratory cell and molecular biology · 2022Article
- Hydrogen sulfide: A new therapeutic target in vascular diseases.Frontiers in endocrinology · 2022Review
- A Case for Hydrogen Sulfide Metabolism as an Oxygen Sensing Mechanism.Antioxidants (Basel, Switzerland) · 2021Review
- The Role of Hydrogen Sulfide in Respiratory Diseases.Biomolecules · 2021Review
- Understanding hydrogen sulfide signaling in neonatal airway disease.Expert review of respiratory medicine · 2021Review
- Bile acids inhibit cholinergic constriction in proximal and peripheral airways from humans and rodents.American journal of physiology. Lung cellular and molecular physiology · 2020Article
- Hydrogen sulfide inhibits CaAmerican journal of physiology. Endocrinology and metabolism · 2019Article
- Cystathionine γ-lyase deficiency enhances airway reactivity and viral-induced disease in mice exposed to side-stream tobacco smoke.Pediatric research · 2019Article
- Redox regulation of ER and mitochondrial CaCell calcium · 2019Review
- Hydrogen sulfide: a gaseous signaling molecule modulates tissue homeostasis: implications in ophthalmic diseases.Cell death & disease · 2019Review
- Alleviation of impaired reactivity in the corpus cavernosum of STZ-diabetic rats by slow-release HInternational journal of impotence research · 2019Article
- A novel GABAAmerican journal of physiology. Lung cellular and molecular physiology · 2019Article
- Airway smooth muscle photorelaxation via opsin receptor activation.American journal of physiology. Lung cellular and molecular physiology · 2019Article
- Attenuation of murine and human airway contraction by a peptide fragment of the cytoskeleton regulatory protein gelsolin.American journal of physiology. Lung cellular and molecular physiology · 2019Article
- Biological Effects of Thermal Water-Associated Hydrogen Sulfide on Human Airways and Associated Immune Cells: Implications for Respiratory Diseases.Frontiers in public health · 2019Review
- Purinergic receptor stimulation induces calcium oscillations and smooth muscle contraction in small pulmonary veins.The Journal of physiology · 2018Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Hydrogen sulphide (H2S) is a signalling molecule that appears to regulate diverse cell physiological process in several organs and systems including vascular and airway smooth muscle cell (SMC) contraction. Decreases in endogenous H2S synthesis have been associated with the development of cardiovascular diseases and asthma. Here we investigated the mechanism of airway SMC relaxation induced by H2S in small intrapulmonary airways using mouse lung slices and confocal and phase-contrast video microscopy. Exogenous H2S donor Na2S (100 μm) reversibly inhibited Ca(2+) release and airway contraction evoked by inositol-1,4,5-trisphosphate (InsP3) uncaging in airway SMCs. Similarly, InsP3-evoked Ca(2+) release and contraction was inhibited by endogenous H2S precursor l-cysteine (10 mm) but not by l-serine (10 mm) or either amino acid in the presence of dl-propargylglycine (PPG). Consistent with the inhibition of Ca(2+) release through InsP3 receptors (InsP3Rs), Na2S reversibly inhibited acetylcholine (ACh)-induced Ca(2+) oscillations in airway SMCs. In addition, Na2S, the H2S donor GYY-4137, and l-cysteine caused relaxation of airways pre-contracted with either ACh or 5-hydroxytryptamine (5-HT). Na2S-induced airway relaxation was resistant to a guanylyl cyclase inhibitor (ODQ) and a protein kinase G inhibitor (Rp-8-pCPT-cGMPS). The effects of H2S on InsP3-evoked Ca(2+) release and contraction as well as on the relaxation of agonist-contracted airways were mimicked by the thiol-reducing agent dithiothreitol (DTT, 10 mm) and inhibited by the oxidizing agent diamide (30 μm). These studies indicate that H2S causes airway SMC relaxation by inhibiting Ca(2+) release through InsP3Rs and consequent reduction of agonist-induced Ca(2+) oscillations in SMCs. The results suggest a novel role for endogenously produced H2S that involves the modulation of InsP3-evoked Ca(2+) release - a cell-signalling system of critical importance for many physiological and pathophysiological processes.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.