Hydrogen sulfide: Regulatory role on blood pressure in hyperhomocysteinemia

Sowmya, Sagiraju; Yada, Swathi; Yeo, Ai Ling; Shoon, Mei Leng; Moore, Philip K.; Bhatia, Madhav

doi:10.1016/j.vph.2010.05.004

Cited by 33 publications

(18 citation statements)

References 46 publications

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“…Cardiovascular system Identical responses to hypoxia and H 2 S, be it constriction, dilation, or multi-phasic, have been observed in more than 30 studies on isolated vessels, perfused organs, and intact animals encompassing all classes of vertebrates (27,94,123,125,128,129,150,151). Not surprisingly, H 2 S also dilates the mouse ductus arteriosus (5), which would be expected to keep this vessel patent in the relative hypoxic intrauterine environment.…”

Section: Physiological Evidence For H 2 S-mediated O 2 Sensingmentioning

confidence: 99%

Hydrogen sulfide as an oxygen sensor

Olson

2013

Clinical Chemistry and Laboratory Medicine

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Significance: Although oxygen (O 2 )-sensing cells and tissues have been known for decades, the identity of the O 2 -sensing mechanism has remained elusive. Evidence is accumulating that O 2 -dependent metabolism of hydrogen sulfide (H 2 S) is this enigmatic O 2 sensor. Recent Advances: The elucidation of biochemical pathways involved in H 2 S synthesis and metabolism have shown that reciprocal H 2 S/O 2 interactions have been inexorably linked throughout eukaryotic evolution; there are multiple foci by which O 2 controls H 2 S inactivation, and the effects of H 2 S on downstream signaling events are consistent with those activated by hypoxia. H 2 S-mediated O 2 sensing has been demonstrated in a variety of O 2 -sensing tissues in vertebrate cardiovascular and respiratory systems, including smooth muscle in systemic and respiratory blood vessels and airways, carotid body, adrenal medulla, and other peripheral as well as central chemoreceptors. Critical Issues: Information is now needed on the intracellular location and stoichometry of these signaling processes and how and which downstream effectors are activated by H 2 S and its metabolites. Future Directions: Development of specific inhibitors of H 2 S metabolism and effector activation as well as cellular organelle-targeted compounds that release H 2 S in a timeor environmentally controlled way will not only enhance our understanding of this signaling process but also provide direction for future therapeutic applications. Antioxid. Redox Signal. 22, 377-397.

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Section: Physiological Evidence For H 2 S-mediated O 2 Sensingmentioning

confidence: 99%

Hydrogen sulfide as an oxygen sensor

Olson

2013

Clinical Chemistry and Laboratory Medicine

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“…Endogenous H 2 S is generated from cysteine metabolism through 2 enzymes: cystathionine-β-synthase and cystathionine-γ-lyase whose productions are mainly in the brain for the former and largely in the cardiovascular system for the latter [13,14]. Growing evidence shows that H 2 S is an important signalling molecule in various body systems, and it gives beneficial effects in animal models of inflammation, hypertension, and ischemia/reperfusion injury inducing anti-inflammatory, cytoprotective, immunomodulating and trophic effects [10,[13][14][15][16][17][18]. The relatively high endogenous concentrations of H 2 S in the brain suggest a neuromodulator role [19]; yet, to date, the detailed mechanisms involved have remained unknown.…”

Section: Mechanisms Of Hydrogenmentioning

confidence: 99%

Mechanisms of Hydrogen Sulfide against the Progression of Severe Alzheimer’s Disease in Transgenic Mice at Different Ages

et al. 2018

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Backgroud: Alzheimer disease is an age-related severe neurodegenerative pathology. The level of the third endogenous gas, hydrogen sulfide (H₂S), is decreased in the brain of Alzheimer’s disease (AD) patients compared with the brain of the age-matched normal individuals; also, plasma H₂S levels are negatively correlated with the severity of AD. Recently, we have demonstrated that systemic H₂S injections are neuroprotective in an early phase of preclinical AD. Objectives: This study focuses on the possible neuroprotection of a chronic treatment with an H₂S donor and sulfurous water (rich of H₂S) in a severe transgenic 3×Tg-AD mice model. Method: 3×Tg-AD mice at 2 different ages (6 and 12 months) were daily treated intraperitoneally with an H₂S donor and sulfurous water (rich of H₂S) for 3 months consecutively. We investigated the cognitive ability, brain morphological alterations, amyloid/tau cascade, excitotoxic, inflammatory and apoptotic responses. Results: Three months of treatments with H₂S significantly protected against impairment in learning and memory in a severe 3×Tg-AD mice model, at both ages studied, and reduced the size of Amyloid β plaques with preservation of the morphological picture. This neuroprotection appeared mainly in the cortex and hippocampus, associated with reduction in activity of c-jun N-terminal kinases, extracellular signal-regulated kinases and p38, which have an established role not only in the phosphorylation of tau protein but also in the inflammatory and excitotoxic response. Conclusion: Our findings indicate that appropriate treatments with various sources of H₂S, might represent an innovative approach to counteract early and severe AD progression in humans.

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“…H 2 S dilates blood vessels, controls blood pressure, and protects the heart from ischemiareperfusion injury (48). Most studies investigating vasodilation by H 2 S have been performed in rodents and have examined large arteries, aortic rings, mesenteric arteries, and measured blood pressure (7,32,42). This study was designed to examine the regulation of cerebral arteriole contractility by H 2 S in newborn pigs.…”

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confidence: 99%

Hydrogen sulfide dilates cerebral arterioles by activating smooth muscle cell plasma membrane K_ATP channels

Liang

Adebiyi

Leo

et al. 2011

American Journal of Physiology-Heart and Circulatory Physiology

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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.

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Hydrogen sulfide: Regulatory role on blood pressure in hyperhomocysteinemia

Cited by 33 publications

References 46 publications

Hydrogen sulfide as an oxygen sensor

Hydrogen sulfide as an oxygen sensor

Mechanisms of Hydrogen Sulfide against the Progression of Severe Alzheimer’s Disease in Transgenic Mice at Different Ages

Hydrogen sulfide dilates cerebral arterioles by activating smooth muscle cell plasma membrane K_ATP channels

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Hydrogen sulfide: Regulatory role on blood pressure in hyperhomocysteinemia

Cited by 33 publications

References 46 publications

Hydrogen sulfide as an oxygen sensor

Hydrogen sulfide as an oxygen sensor

Mechanisms of Hydrogen Sulfide against the Progression of Severe Alzheimer’s Disease in Transgenic Mice at Different Ages

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

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Hydrogen sulfide dilates cerebral arterioles by activating smooth muscle cell plasma membrane K_ATP channels