scholarly journals Hydrogen sulfide activates Ca2+sparks to induce cerebral arteriole dilatation

2012 ◽  
Vol 590 (11) ◽  
pp. 2709-2720 ◽  
Author(s):  
Guo Hua Liang ◽  
Qi Xi ◽  
Charles W. Leffler ◽  
Jonathan H. Jaggar
Keyword(s):  
Hydrogen Sulfide ◽  
Cerebral Arteriole

scholarly journals Hydrogen sulfide dilates cerebral arterioles by activating smooth muscle cell plasma membrane KATP channels

2011 ◽  
Vol 300 (6) ◽  
pp. H2088-H2095 ◽  
Author(s):  
Guo Hua Liang ◽  
Adebowale Adebiyi ◽  
M. Dennis Leo ◽  
Elizabeth M. McNally ◽  
Charles W. Leffler ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Hydrogen Sulfide ◽  
Smooth Muscle Cells ◽  
Smooth Muscle Cell ◽  
Muscle Cell ◽  
Muscle Cells ◽  
Mass Spectrometry Data ◽  
Vascular Regulation ◽  
Cerebral Arterioles ◽  
Cerebral Arteriole

Hydrogen sulfide (H2S) 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 H2S exist. Here, we tested the hypothesis that piglet cerebral arteriole smooth muscle cells generate ATP-sensitive K+ (KATP) currents and that H2S induces vasodilation by activating KATP currents. Gas chromatography/mass spectrometry data demonstrated that after placing Na2S, an H2S donor, in solution, it rapidly (1 min) converts to H2S. Patch-clamp electrophysiology indicated that pinacidil (a KATP channel activator), Na2S, and NaHS (another H2S donor) activated K+ currents at physiological steady-state voltage (−50 mV) in isolated cerebral arteriole smooth muscle cells. Glibenclamide, a selective KATP channel inhibitor, fully reversed pinacidil-induced K+ currents and partially reversed (∼58%) H2S-induced K+ currents. Western blot analysis indicated that piglet arterioles expressed inwardly rectifying K+ 6.1 (Kir6.1) channel and sulfonylurea receptor 2B (SUR2B) KATP channel subunits. Pinacidil dilated pressurized (40 mmHg) piglet arterioles, and glibenclamide fully reversed this effect. Na2S also induced reversible and repeatable vasodilation with an EC50 of ∼30 μM, and this effect was partially reversed (∼55%) by glibenclamide. Vasoregulation by H2S was also studied in pressurized resistance-size cerebral arteries of mice with a genetic deletion in the gene encoding SUR2 (SUR2 null). Pinacidil- and H2S-induced vasodilations were smaller in arterioles of SUR2 null mice than in wild-type controls. These data indicate that smooth muscle cell KATP currents control newborn cerebral arteriole contractility and that H2S dilates cerebral arterioles by activating smooth muscle cell KATP channels containing SUR2 subunits.

scholarly journals Hydrogen sulfide activates Ca 2+ sparks to induce cerebral arteriole dilation

2012 ◽  
Vol 26 (S1) ◽  
Author(s):  
Guo Hua Liang ◽  
Qi Xi ◽  
Charles W. Leffler ◽  
Jonathan H. Jaggar
Keyword(s):  
Hydrogen Sulfide ◽  
Cerebral Arteriole

P6 Hydrogen sulfide activates Ca2+ sparks to induce cerebral arteriole dilation

Nitric Oxide ◽  
2012 ◽  
Vol 27 ◽  
pp. S13-S14
Author(s):  
Guohua Liang ◽  
Qi xi ◽  
Charles Leffler ◽  
Jonathan Jaggar
Keyword(s):  
Hydrogen Sulfide ◽  
Cerebral Arteriole

Endogenous hydrogen sulfide sulfhydrates IKKβ at cysteine 179 to control pulmonary artery endothelial cell inflammation

2019 ◽  
Vol 133 (20) ◽  
pp. 2045-2059 ◽  
Author(s):  
Da Zhang ◽  
Xiuli Wang ◽  
Siyao Chen ◽  
Selena Chen ◽  
Wen Yu ◽  
...  
Keyword(s):  
Hydrogen Sulfide ◽  
Endothelial Cell ◽  
Pulmonary Artery ◽  
Cell Model ◽  
Site Directed Mutagenesis ◽  
Critical Event ◽  
Hypertensive Rats ◽  
Pulmonary Artery Endothelial Cell

Abstract Background: Pulmonary artery endothelial cell (PAEC) inflammation is a critical event in the development of pulmonary arterial hypertension (PAH). However, the pathogenesis of PAEC inflammation remains unclear. Methods: Purified recombinant human inhibitor of κB kinase subunit β (IKKβ) protein, human PAECs and monocrotaline-induced pulmonary hypertensive rats were employed in the study. Site-directed mutagenesis, gene knockdown or overexpression were conducted to manipulate the expression or activity of a target protein. Results: We showed that hydrogen sulfide (H2S) inhibited IKKβ activation in the cell model of human PAEC inflammation induced by monocrotaline pyrrole-stimulation or knockdown of cystathionine γ-lyase (CSE), an H2S generating enzyme. Mechanistically, H2S was proved to inhibit IKKβ activity directly via sulfhydrating IKKβ at cysteinyl residue 179 (C179) in purified recombinant IKKβ protein in vitro, whereas thiol reductant dithiothreitol (DTT) reversed H2S-induced IKKβ inactivation. Furthermore, to demonstrate the significance of IKKβ sulfhydration by H2S in the development of PAEC inflammation, we mutated C179 to serine (C179S) in IKKβ. In purified IKKβ protein, C179S mutation of IKKβ abolished H2S-induced IKKβ sulfhydration and the subsequent IKKβ inactivation. In human PAECs, C179S mutation of IKKβ blocked H2S-inhibited IKKβ activation and PAEC inflammatory response. In pulmonary hypertensive rats, C179S mutation of IKKβ abolished the inhibitory effect of H2S on IKKβ activation and pulmonary vascular inflammation and remodeling. Conclusion: Collectively, our in vivo and in vitro findings demonstrated, for the first time, that endogenous H2S directly inactivated IKKβ via sulfhydrating IKKβ at Cys179 to inhibit nuclear factor-κB (NF-κB) pathway activation and thereby control PAEC inflammation in PAH.

Limnological characteristics, community metabolism and management strategies of a coastal sinkhole in Cuba (Cenote Jennifer)

2020 ◽  
Vol 56 ◽  
pp. 24
Author(s):  
Roberto González-De Zayas ◽  
Liosban Lantigua Ponce de León ◽  
Liezel Guerra Rodríguez ◽  
Felipe Matos Pupo ◽  
Leslie Hernández-Fernández
Keyword(s):  
Hydrogen Sulfide ◽  
Primary Productivity ◽  
Major Ions ◽  
Saline Water ◽  
Management Strategies ◽  
Tourist Destination ◽  
Community Metabolism ◽  
Morphological Studies ◽  
Made In ◽  
Limnological Parameters

The Cenote Jennifer is an important and unique aquatic sinkhole in Cayo Coco (Jardines del Rey Tourist Destination) that has brackish to saline water. Two samplings were made in 1998 and 2009, and 4 metabolism community experiments in 2009. Some limnological parameters were measured in both samplings (temperature, salinity, pH, dissolved oxygen major ions, hydrogen sulfide, nutrients and others). Community metabolism was measured through incubated oxygen concentration in clear and dark oxygen bottles. Results showed that the sinkhole limnology depends on rainfall and light incidence year, with some stratification episodes, due to halocline or oxycline presence, rather than thermocline. The sinkhole water was oligotrophic (total nitrogen of 41.5 ± 22.2 μmol l−1 and total phosphorus of 0.3 ± 0.2 μmol l−1) and with low productivity (gross primary productivity of 63.0 mg C m−2 d−1). Anoxia and hypoxia were present at the bottom with higher levels of hydrogen sulfide, lower pH and restricted influence of the adjacent sea (2 km away). To protect the Cenote Jennifer, tourist exploitation should be avoided and more resources to ecological and morphological studies should be allocated, and eventually use this aquatic system only for specialized diving. For conservation purposes, illegal garbage disposal in the surrounding forest should end.

Effect of Hydrogen Sulfide on Reactions of Isolated Rat Heart under Volume Load and Ischemia-Reperfusion

2013 ◽  
Vol 4 (3) ◽  
pp. 201-212
Author(s):  
Tetyana V Shimanskaya ◽  
Yulia V. Goshovska ◽  
Olena M. Semenykhina ◽  
Vadim F. Sagach
Keyword(s):  
Hydrogen Sulfide ◽  
Rat Heart ◽  
Ischemia Reperfusion ◽  
Isolated Rat Heart ◽  
Volume Load ◽  
Isolated Rat
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