Hydrogen sulfide inhibits endothelial nitric oxide formation and receptor ligand-mediated Ca2+ release in endothelial and smooth muscle cells

Kloesch, Burkhard; Steiner, Günter; Mayer, Bernd; Schmidt, Kurt

doi:10.1016/j.pharep.2015.05.026

Cited by 16 publications

(12 citation statements)

References 36 publications

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“…It has been suggested that H 2 S and NO are required in endothelium-dependent vasorelaxation in isolated aortic ring (Coletta et al, 2012). In human endothelial cells and smooth muscle cells from rat aorta, H 2 S limited the formation of NO (Kloesch et al, 2016). Accordingly, in the present study a negative correlation between the NO and H 2 S groups was observed in the male group.…”

Section: Discussionsupporting

confidence: 55%

Age- and sex-dependent alteration of functions and epigenetic modifications of vessel and endothelium related biomarkers

Han¹,

Aydın²,

Akansel³

et al. 2018

Turk J Biol

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Introduction Aging is a natural process for every living organism. The trouble here is increased health problems as a result of aging. Aging is a dominant risk factor for cardiovascular diseases and is associated with progressive vascular dysfunction (Herrera et al., 2010; Laurent, 2012). Many studies reported a sex difference in age-associated vascular changes (Sarabi et al., 1999; Sader and Celermajer, 2002; Okumura et al., 2011). Celermajer et al. (1994) showed that age-related impairment in endothelial function appeared to occur earlier in males than in females. Different regulation of endothelial function is one of the main mechanisms underlying the variation in age-associated vascular changes in females and males (Sarabi et al., 1999). However, the underlying mechanisms of sex-dependent alterations in endothelial function remain to be investigated. Endothelium-derived NO plays a key role in the regulation of vascular homeostasis (Moncada et al., 1991). The capacity of NO release is considered to be a major indicator of endothelial function. Vascular aging characterized by endothelial dysfunction is associated with reduced NO bioavailability and increased generation of reactive oxygen species (ROS). ROS combine with NO and produce deleterious free radicals, leading to endothelial dysfunction (Heitzer et al., 2001; Tsimakis, 2006; El Assar et al., 2013; Rochette et al., 2013). ADMA is an endogenous competitive inhibitor of NO synthase and an increase in ADMA is associated with impairment of NO synthesis (Bouras et al., 2013; Sverdlov et al., 2014). It has been reported that plasma concentrations of ADMA increase in elderly people and in postmenopausal women (Schulze et al., 2005). H 2 S is acknowledged as an important gaseous signaling molecule (Kolluru et al., 2013). It has been revealed that H 2 S is an endogenous regulator of oxidative damage and aging in C. elegans (Qabazard et al., 2014). However, the relationship between these molecules and endothelial function in the aging process is still largely unknown. Recent studies have focused on epigenetic changes that occur as a hallmark of aging (Brunet and Berger, 2014).

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Section: Discussionsupporting

confidence: 55%

Age- and sex-dependent alteration of functions and epigenetic modifications of vessel and endothelium related biomarkers

Han¹,

Aydın²,

Akansel³

et al. 2018

Turk J Biol

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“…; Kloesch et al. ; Blatter ), and autonomic neurotransmitters such as norepinephrine (Garssen et al. ) that affect ASM.…”

Section: Discussionmentioning

confidence: 99%

“…Although this study carefully investigated the influence of cholinergic nerves which play a predominant role, it is worth noting that other cell types, such as airway epithelial cells (Vanhoutte 2013) and sympathetic nerves (van Nieuwstadt et al 1994), can release factors in response to chemical depolarization that influence contractility of tracheal smooth muscle cells. These are factors released from tissue such as prostaglandins and nitric oxide (Ruan et al 2011;Kloesch et al 2016;Blatter 2017), and autonomic neurotransmitters such as norepinephrine (Garssen et al 1990) that affect ASM. Under conditions where we attempted to isolate depolarization-mediated effects, then 0 calcium external solution would be expected to prevent depolarization-induced secretion of these factors or sympathetic neurotransmitter release (Atlas 2001).…”

Section: Zero Ca2 + External Solution and Nifedipine Isolates Contracmentioning

confidence: 99%

Voltage effects on muscarinic acetylcholine receptor‐mediated contractions of airway smooth muscle

Semenov

Brenner

2018

Physiol Rep

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Studies have shown that the activity of muscarinic receptors and their affinity to agonists are sensitive to membrane potential. It was reported that in airway smooth muscle (ASM) depolarization evoked by high K+ solution increases contractility through direct effects on M3 muscarinic receptors. In this study, we assessed the physiological relevance of voltage sensitivity of muscarinic receptors on ASM contractility. Our findings reveal that depolarization by high K+ solution induces contraction in intact mouse trachea predominantly through activation of acetylcholine release from embedded nerves, and to a lesser extent by direct effects on M3 receptors. We therefore devised a pharmacological approach to depolarize tissue to various extents in an organ bath preparation, and isolate contraction due exclusively to ASM muscarinic receptors within range of physiological voltages. Our results indicate that unliganded muscarinic receptors do not contribute to contraction regardless of voltage. Utilizing low K+ solution to hyperpolarize membrane potentials during contractions had no effect on liganded muscarinic receptor‐evoked contractions, although it eliminated the contribution of voltage‐gated calcium channels. However, we found that muscarinic signaling was potentiated by at least 42% at depolarizing voltages (average −12 mV) induced by high K+ solution (20 mmol/L K+). In summary, we conclude that contractions evoked by direct activation of muscarinic receptors have negligible sensitivity to physiological voltages. However, contraction activated by cholinergic stimulation can be potentiated by membrane potentials occurring beyond the physiological range of ASM.

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“…It can also directly boost eNOS activity through S-sulfhydration, and by promoting endothelial influx of calcium via activation of TRPV1 channels 41 46. However, as a countervailing effect, H 2 S can inhibit endothelial eNOS activation by certain agonists owing to its ability to suppress inositol-1,4,5-triphosphate-mediated release of calcium from intracellular stores 51 52. The same mechanism opposes vasoconstriction of smooth muscle and platelet aggregation 52.…”

Section: Endogenous Hydrogen Sulfide Production Confers Versatile Carmentioning

confidence: 99%

Boosting endogenous production of vasoprotective hydrogen sulfide via supplementation with taurine and N-acetylcysteine: a novel way to promote cardiovascular health

2017

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Hydrogen sulfide inhibits endothelial nitric oxide formation and receptor ligand-mediated Ca2+ release in endothelial and smooth muscle cells

Abstract: H2S antagonized Ca(2+) mobilization by receptor agonists and store-operated Ca(2+) entry thereby limiting eNOS activation and NO formation. The effect of H2S on Ca(2+) stores was not restricted to endothelial cells but was also observed in vascular and tracheal smooth muscle cells.

Cited by 16 publications

References 36 publications

Age- and sex-dependent alteration of functions and epigenetic modifications of vessel and endothelium related biomarkers

Age- and sex-dependent alteration of functions and epigenetic modifications of vessel and endothelium related biomarkers

Voltage effects on muscarinic acetylcholine receptor‐mediated contractions of airway smooth muscle

Boosting endogenous production of vasoprotective hydrogen sulfide via supplementation with taurine and N-acetylcysteine: a novel way to promote cardiovascular health

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