ArticleAmerican journal of physiology. Heart and circulatory physiology2011
Hydrogen sulfide dilates cerebral arterioles by activating smooth muscle cell plasma membrane KATP channels.
Article in American journal of physiology. Heart and circulatory physiology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 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
39 citing papers in PubMed, 71 citations in OpenAlex.
- Potassium channels in vascular smooth muscle cells.Physiological reviews · 2026Review
- The Role of Hydrogen Sulfide in Peripheral Nervous System Modulation.Handbook of experimental pharmacology · 2026Review
- Effect of Hydrogen Sulfide on Sympathoinhibition in Obese Pithed Rats and Participation of KInternational journal of hypertension · 2024Article
- Cerebroprotective actions of hydrogen sulfide in the epileptic brain in newborn pigs.Pediatric research · 2023Article
- Review
- Potential Effects of Natural HBiomolecules · 2022Review
- Hydrogen Sulfide-Induced Vasodilation: The Involvement of Vascular Potassium Channels.Frontiers in pharmacology · 2022Review
- Regulation of the Cerebral Circulation During Development.Comprehensive Physiology · 2021Article
- The Potential Role of Hydrogen Sulfide in the Regulation of Cerebrovascular Tone.Biomolecules · 2020Review
- Hydrogen Sulfide Relaxes Human Uterine Artery via Activating Smooth Muscle BKAntioxidants (Basel, Switzerland) · 2020Article
- Vasodilator effects of sulforaphane in cerebral circulation: A critical role of endogenously produced hydrogen sulfide and arteriolar smooth muscle KJournal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2020Article
- Vasorelaxation elicited by endogenous and exogenous hydrogen sulfide in mouse mesenteric arteries.Naunyn-Schmiedeberg's archives of pharmacology · 2020Article
- Hydrogen Sulfide in Pharmacotherapy, Beyond the Hydrogen Sulfide-Donors.Biomolecules · 2020Review
- The role of gasotransmitters in neonatal physiology.Nitric oxide : biology and chemistry · 2020Review
- HAmerican journal of physiology. Heart and circulatory physiology · 2018Article
- Regulation of vascular tone homeostasis by NO and HBiochemical pharmacology · 2018Review
- The Role of Gaseous Molecules in Traumatic Brain Injury: An Updated Review.Frontiers in neuroscience · 2018Review
- Article
- Beyond a Gasotransmitter: Hydrogen Sulfide and Polysulfide in Cardiovascular Health and Immune Response.Antioxidants & redox signaling · 2017Review
- Vascular biology of hydrogen sulfide.American journal of physiology. Cell physiology · 2017Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
Hydrogen sulfide (H(2)S) is a gaseous signaling molecule that appears to contribute to the regulation of vascular tone and blood pressure. Multiple potential mechanisms of vascular regulation by H(2)S exist. Here, we tested the hypothesis that piglet cerebral arteriole smooth muscle cells generate ATP-sensitive K(+) (K(ATP)) currents and that H(2)S induces vasodilation by activating K(ATP) currents. Gas chromatography/mass spectrometry data demonstrated that after placing Na(2)S, an H(2)S donor, in solution, it rapidly (1 min) converts to H(2)S. Patch-clamp electrophysiology indicated that pinacidil (a K(ATP) channel activator), Na(2)S, and NaHS (another H(2)S donor) activated K(+) currents at physiological steady-state voltage (-50 mV) in isolated cerebral arteriole smooth muscle cells. Glibenclamide, a selective K(ATP) channel inhibitor, fully reversed pinacidil-induced K(+) currents and partially reversed (∼58%) H(2)S-induced K(+) currents. Western blot analysis indicated that piglet arterioles expressed inwardly rectifying K(+) 6.1 (K(ir)6.1) channel and sulfonylurea receptor 2B (SUR2B) K(ATP) channel subunits. Pinacidil dilated pressurized (40 mmHg) piglet arterioles, and glibenclamide fully reversed this effect. Na(2)S also induced reversible and repeatable vasodilation with an EC(50) of ∼30 μM, and this effect was partially reversed (∼55%) by glibenclamide. Vasoregulation by H(2)S was also studied in pressurized resistance-size cerebral arteries of mice with a genetic deletion in the gene encoding SUR2 (SUR2 null). Pinacidil- and H(2)S-induced vasodilations were smaller in arterioles of SUR2 null mice than in wild-type controls. These data indicate that smooth muscle cell K(ATP) currents control newborn cerebral arteriole contractility and that H(2)S dilates cerebral arterioles by activating smooth muscle cell K(ATP) channels containing SUR2 subunits.
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.