Time-dependent interaction between hydrogen sulfide, nitric oxide and sulfur dioxide in the relation of rat aorta

Nitric Oxide ◽  
2015 ◽  
Vol 47 ◽  
pp. S18-S19
Author(s):  
Abbas B.Q. Salihi ◽  
Mudhir S. Shekha ◽  
Omar A.M. Al-Habib
Keyword(s):  
Nitric Oxide ◽  
Hydrogen Sulfide ◽  
Sulfur Dioxide ◽  
Rat Aorta ◽  
Time Dependent ◽  
Dependent Interaction

Sulfur dioxide induces vascular relaxation through PI3K/Akt/eNOS and NO/cGMP signaling pathways in rats

2020 ◽  
Vol 39 (8) ◽  
pp. 1108-1117
Author(s):  
Q Zhang ◽  
W Lyu ◽  
M Yu ◽  
Y Niu
Keyword(s):  
Nitric Oxide ◽  
Sulfur Dioxide ◽  
Signaling Pathways ◽  
Underlying Mechanism ◽  
Cyclic Guanosine Monophosphate ◽  
Rat Aorta ◽  
Guanosine Monophosphate ◽  
Signal Pathways ◽  
Atmospheric Pollutant ◽  
Protein Levels

Sulfur dioxide (SO2) is a common exogenous atmospheric pollutant. Studies have shown that SO2 can cause vasodilation as a gas signaling molecule, but the specific signaling pathways are not well understood. This study aimed to explore the underlying mechanism behind the effects of SO2 on vasodilation of isolated rat aorta. The results showed that when the dose of SO2 was 30 μM, the vasodilation of endothelium-intact rings was partially suppressed by LY294002 and NG-nitro-l-arginine methyl ester, and the protein levels of phosphoinositide 3-kinase (PI3K), p-Akt, and p-endothelial nitric oxide synthase ( p-eNOS) were significantly increased. When the dose of SO2 was 300 μM or 1500 μM, the vasodilation of endothelium-denuded rings did not change after application of the inhibitor, but the protein levels of PI3K, p-Akt, and p-eNOS were significantly decreased, and the activity of NOS and the level of nitric oxide (NO) and cyclic guanosine monophosphate (cGMP) were significantly increased. We speculate that the mechanism of SO2-induced vasodilatation likely involved the endothelial PI3K/Akt/eNOS and NO/cGMP signal pathways. In addition, at the concentration of 1500 μM, SO2 markedly increased the level of caspase-3 and caspase-9. The results suggest that high concentrations of SO2 may cause damage to blood vessels. This study will help to further inform the etiologies of SO2-related cardiovascular disease.

Stimulation of the endogenous hydrogen sulfide synthesis suppresses oxidative–nitrosative stress and restores endothelial-dependent vasorelaxation in old rats

2020 ◽  
Vol 98 (5) ◽  
pp. 275-281 ◽  
Author(s):  
L.A. Mys ◽  
N.A. Strutynska ◽  
Y.V. Goshovska ◽  
V.F. Sagach
Keyword(s):  
Nitric Oxide ◽  
Hydrogen Sulfide ◽  
Nitric Oxide Synthase ◽  
Vascular Reactivity ◽  
Nitrosative Stress ◽  
Rat Aorta ◽  
Aortic Tissue ◽  
Old Rats ◽  
Oxide Synthase ◽  
Stimulation Of

Hydrogen sulfide (H2S) is an endogenous gas transmitter with profound effects on the cardiovascular system. We hypothesized that stimulation of H2S synthesis might alleviate age-associated changes in vascular reactivity. Pyridoxal-5-phosphate (PLP), the coenzyme of H2S-synthesizing enzymes, was administrated to old male Wistar rats per os at a dose of 0.7 mg/kg body mass once a day for 2 weeks. H2S content in the aortic tissue, markers of oxidative stress, inducible nitric oxide synthase (iNOS) and constitutive nitric oxide synthase (cNOS), arginase activities, and endothelium-dependent vasorelaxation of the aortic rings were studied. Our results showed that PLP restored endogenous H2S and low molecular weight S-nitrosothiol levels in old rat aorta to the levels detected in adults. PLP significantly reduced diene conjugate content, hydrogen peroxide and peroxynitrite generation rates, and iNOS and arginase activity in the aortic tissue of old rats. PLP also greatly improved acetylcholine-induced relaxation of old rat aorta (47.7% ± 4.8% versus 18.4% ± 4.1% in old rats, P < 0.05) that was abolished by NO inhibition with N-nitro-l-arginine methyl ester hydrochloride (L-NAME) or H2S inhibition with O-carboxymethylhydroxylamine (O-CMH). Thus, PLP might be used for stimulation of endogenous H2S synthesis and correction of oxidative and nitrosative stress and vessel tone dysfunction in aging and age-associated diseases.

Vasorelaxant Effect of Novel Nitric Oxide-Hydrogen Sulfide Donor Chalcone in Isolated Rat Aorta: Involvement of cGMP Mediated sGC and Potassium Channel Activation

2020 ◽  
Vol 13 (2) ◽  
pp. 126-136
Author(s):  
Amol Sherikar ◽  
Rakesh Dhavale ◽  
Manish Bhatia
Keyword(s):  
Nitric Oxide ◽  
Methylene Blue ◽  
Hydrogen Sulfide ◽  
Potassium Channel ◽  
Rat Aorta ◽  
Tetraethylammonium Chloride ◽  
Vasorelaxant Effect ◽  
Activation Assay ◽  
Isolated Rat

Background and Objective: : Recently, nitric oxide (NO) and hydrogen sulfide (H2S) donating moieties were extensively studied for their role in the vasculature as they are responsible for many cellular and pathophysiological functioning. The objective of the present study is to evaluate novel NO and H2S donating chalcone moieties on isolated rat aorta for vasorelaxation, and to investigate the probable mechanism of action. Methods:: To extend our knowledge of vasorelaxation by NO and H2S donor drugs, here we investigated the vasorelaxing activity of novel NO and H2S donating chalcone moieties on isolated rat aorta. The mechanism of vasorelaxation by these molecules was investigated by performing in vitro cGMP mediated sGC activation assay and using Tetraethylammonium chloride (TEA) as a potassium channel blocker and Methylene blue as NO blocker. Results:: Both NO and H2S donating chalcone moieties were found to be potent vasorelaxant. The compound G4 and G5 produce the highest vasorelaxation with 3.716 and 3.789 M of pEC50, respectively. After the addition of TEA, G4 and G5 showed 2.772 and 2.796 M of pEC50, respectively. The compounds Ca1, Ca2, and D7 produced significant activation and release of cGMP mediated sGC which was 1.677, 1.769 and 1.768 M of pEC50, respectively. Conclusion: : The vasorelaxation by NO-donating chalcones was blocked by Methylene blue but it did not show any effect on H2S donating chalcones. The vasorelaxing potency of NO-donating molecules was observed to be less affected by the addition of TEA but H2S donors showed a decrease in both efficacy and potency. The cGMP release was more in the case of NO-donating molecules. The tested compounds were found potent for relaxing vasculature of rat aorta.

Bicarbonate-dependent effect of hydrogen sulfide on vascular contractility in rat aortic rings

2010 ◽  
Vol 299 (4) ◽  
pp. C866-C872 ◽  
Author(s):  
Yi-Hong Liu ◽  
Jin-Song Bian
Keyword(s):  
Nitric Oxide ◽  
Hydrogen Sulfide ◽  
Anion Exchanger ◽  
Rat Aorta ◽  
Disulfonic Acid ◽  
Dependent Effect ◽  
Nitric Oxide Level ◽  
Adrenoceptor Agonist ◽  
Anion Exchanger 2 ◽  
First Time

Hydrogen sulfide (H2S), an endogenous gaseous mediator, produces both vasorelaxation and vasoconstriction at different concentrations. We found in the present study that NaHS, an H2S donor, produced stronger vasorelaxant and weaker vasoconstrictive effects in HEPES solution compared with those achieved in Krebs solution. We further screened the buffer components and found that bicarbonate (HCO3−) was the ion to influence the effect of H2S. After examining the vasorelaxant effects of acetylcholine, a vasodilator by releasing nitric oxide, and isoprenaline, a β-adrenoceptor agonist, in HEPES and Krebs buffers, we found the HCO3−-dependent effect was specific to H2S. Blockade of anion exchanger-2 activity with 4,4′-diisothiocyanatostilbene-2,2′-disulfonic acid (DIDS) or with HCO3−-free solution abolished the vasoconstrictive effect of NaHS. Moreover, NaHS decreased nitric oxide level in the rat aorta in HCO3−-containing buffer, but this effect was abolished by HCO3−-free buffer or DIDS. In summary, we found for the first time that H2S stimulates anion exchanger to transport extracellular HCO3− in exchange for intracellular superoxide anions, which may further inactivate nitric oxide and induces vasoconstriction.

Infrared Spectrophotometric Analysis of Medicinal Gases for Trace Impurities

1976 ◽  
Vol 59 (6) ◽  
pp. 1404-1408
Author(s):  
Wilson L Brannon ◽  
Walter R Benson ◽  
George Schwartzman
Keyword(s):  
Nitric Oxide ◽  
Carbon Dioxide ◽  
Carbon Monoxide ◽  
Hydrogen Sulfide ◽  
Sulfur Dioxide ◽  
Spectrophotometric Analysis ◽  
Gas Cell ◽  
Trace Impurities ◽  
Infrared Spectrophotometer ◽  
Low Levels

Abstract The feasibility of examining medicinal gases for trace impurities, using an infrared spectrophotometer in conjunction with a 10 m gas cell, was investigated. Many of the impurities for which the USP includes limits were detected and measured at concentrations at or below those permitted by the USP; these include sulfur dioxide, carbon dioxide, carbon monoxide, and water. However, others (hydrogen sulfide, nitric oxide, and nitrogen dioxide) were not detected at these levels by this technique. Methane was found at low levels in some samples.

CHANGES OF NITRIC OXIDE SYNTHASE AND HYDROGEN SULFIDE IN BLOOD LYMPHOCYTES IN THE ACUTE PERIOD OF POLYTRAUMA

2019 ◽  
Vol 72 (8) ◽  
pp. 1473-1476
Author(s):  
Nataliya Matolinets ◽  
Helen Sklyarova ◽  
Eugene Sklyarov ◽  
Andrii Netliukh
Keyword(s):  
Nitric Oxide ◽  
Hydrogen Sulfide ◽  
Tissue Injury ◽  
Traumatic Injury ◽  
Cell Types ◽  
No Synthase ◽  
Septic Complications ◽  
Acute Period ◽  
Gaseous Transmitters ◽  
The Moment

Introduction: Polytrauma patients have high risk of shock, septic complications and death during few years of follow-up. In recent years a lot of attention is paid to gaseous transmitters, among which are nitrogen oxide (NO) and hydrogen sulfide (H2S). It is known that the rise of NO and its metabolites levels occurs during the acute period of polytrauma. Nitric oxide and hydrogen sulfide are produced in different cell types, among which are lymphocytes. The aim: To investigate the levels of NO, NOS, iNOS, еNOS, H2S in lymphocytes lysate in patients at the moment of hospitalization and 24 hours after trauma. Materials and methods: We investigated the levels of NO, NO-synthase, inducible NO-synthase, endothelial NO-synthase, H2S in lymphocytes lysate in patients at the moment of hospitalization and 24 hours after trauma. Results: The study included 20 patients with polytrauma who were treated in the intensive care unit (ICU) of the Lviv Emergency Hospital. Tissue injury was associated with an increased production of NO, NOS, iNOS, еNOS during the acute period of polytrauma. At the same time, the level of H2S decreased by the end of the first day of traumatic injury. Conclusions: In acute period of polytrauma, significant increasing of iNOS and eNOS occurs with percentage prevalence of iNOS over eNOS on the background of H2S decreasing.

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