Hydrogen sulfide upregulates KATP channel expression in vascular smooth muscle cells of spontaneously hypertensive rats

Sun, Yan; Huang, Yaqian; Zhang, Rongyuan; Chen, Qinghua; Chen, Jie; Zong, Yanfang; Liu, Jia; Feng, Shasha; Liu, Angie Dong; Holmberg, L. Joakim; Liu, Die; Tang, Chaoshu; Du, Junbao; Jin, Hongfang

doi:10.1007/s00109-014-1227-1

Cited by 60 publications

(50 citation statements)

References 44 publications

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“…We did not measure serum H 2 S in the present study due to the aforementioned methodological difficulties and instead favored measurement of tissue-specific H 2 S production from the substrates for CSE and 3-MPST, L-cysteine and 3-MP, respectively. Our findings are consistent with those observed in rodent models of hypertension, in which expression and activity of H 2 S-producing enzymes are reduced and contribute to vascular dysfunction 4, 12, 13, 39 .…”

Section: Discussionsupporting

confidence: 91%

“…Moreover, long-term systemic treatment with a H 2 S donor improves endothelial function in hypertensive rodents, in part, via increased NO bioavailability 12, 14, 15, 39 , suggesting that the loss of redundancy and synergism between the NO and H 2 S signaling pathways contributes to vascular dysfunction in hypertension 5, 11, 43 . In this regard, endogenous H 2 S appears to be required for the full vasodilatory actions of NO.…”

Section: Discussionmentioning

confidence: 99%

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Impaired Hydrogen Sulfide–Mediated Vasodilation Contributes to Microvascular Endothelial Dysfunction in Hypertensive Adults

et al. 2017

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Reductions in hydrogen sulfide (H2S) production have been implicated in the pathogenesis of vascular dysfunction in animal models of hypertension; however, no studies have examined a functional role for H2S contributing to microvascular dysfunction in hypertensive (HTN) adults. We hypothesized that endogenous production of H2S would be reduced, impaired endothelium-dependent vasodilation would be mediated by reductions in H2S-dependent vasodilation, and vascular responsiveness to exogenous H2S (Na2S) would be attenuated in HTN compared to normotensive (NTN) adults. Fifteen NTN [51±2 yrs; blood pressure (BP) 116±3/76±3 mmHg] and 14 HTN adults (57±2 yrs; BP 140±3/89±2 mmHg) participated. H2S biosynthetic enzyme expression (Western blot) and substrate-dependent H2S production (amperometric probe) were measured in cutaneous tissue homogenates. Red cell flux (laser Doppler flowmetry) was measured during graded perfusions of acetylcholine (ACh; 10−6 –10−1 mol∙L−1) and Na2S (10−5–101 mol∙L−1) using intradermal microdialysis; the functional role of H2S was determined using pharmacological inhibition with aminooxyacetic acid (AOAA; 0.5 mmol∙L−1). H2S biosynthetic enzyme expression and substrate-dependent H2S production were reduced in HTN adults (all p<0.05). ACh-induced endothelium-dependent vasodilation was blunted in HTN compared to NTN adults (p=0.012). AOAA attenuated ACh-induced vasodilation in NTN adults (ACh: 1.31±0.13 vs. ACh+AOAA: 1.07±0.09 flux∙mmHg−1; P=0.025) but had no effect on vasodilation in HTN adults (ACh: 1.16±0.10 v. ACh+AOAA: 1.37±0.11 flux∙mmHg−1; p=0.47). Na2S-induced vasodilation was not different between groups. Collectively, these findings indicate that while the microvasculature maintains the ability to vasodilate in response to exogenous H2S, reductions in endogenous synthesis and H2S-dependent vasodilation contribute to endothelial dysfunction in human hypertension.

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Section: Discussionsupporting

confidence: 91%

Section: Discussionmentioning

confidence: 99%

Impaired Hydrogen Sulfide–Mediated Vasodilation Contributes to Microvascular Endothelial Dysfunction in Hypertensive Adults

et al. 2017

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“…Administration of NaHS to cardiomyocytes increased glucose uptake by these cells [174, 175], increased the phosphorylation of several components of the insulin/IGF-1 signal pathway, like insulin receptor, PI3K and Akt [175], and improved glucose metabolism [174, 176]. H 2 S regulated vaso-relaxation in spontaneously hypertensive rats through the inhibition of FOXO1 and FOXO3 phosphorylation, which resulted in their nuclear translocation and their binding to target gene promotors [177]. H 2 S was also shown to function as an endogenous regulator of PTEN, the main antagonist of the PI3K-Akt axis in the insulin/IGF-1 signal pathway, by modifying PTEN activity through S-sulfhydration [178, 179].…”

Section: Hydrogen Sulfide and Agingmentioning

confidence: 99%

The role of hydrogen sulfide in aging and age-related pathologies

Perridon

Leuvenink

Hillebrands

et al. 2016

Aging

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When humans grow older, they experience inevitable and progressive loss of physiological function, ultimately leading to death. Research on aging largely focuses on the identification of mechanisms involved in the aging process. Several proposed aging theories were recently combined as the ‘hallmarks of aging’. These hallmarks describe (patho-)physiological processes that together, when disrupted, determine the aging phenotype. Sustaining evidence shows a potential role for hydrogen sulfide (H2S) in the regulation of aging.Nowadays, H2S is acknowledged as an endogenously produced signaling molecule with various (patho-) physiological effects. H2S is involved in several diseases including pathologies related to aging. In this review, the known, assumed and hypothetical effects of hydrogen sulfide on the aging process will be discussed by reviewing its actions on the hallmarks of aging and on several age-related pathologies.

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“…H 2 S may decrease hypertension by opening voltage-dependent potassium channels, resulting in vasorelaxation and increasing vascular tone through multiple mechanisms (77,125). H 2 S also induces vasorelaxation by opening K ATP channels (136,162) and increasing NO production (38). Contrary to vasorelaxation, Na 2 S and NaHS increased intracavernosal pressure by opening potassium channels in penile tissue (68), suggesting that H 2 S may cause vasoconstriction in other tissues.…”

Section: Diabetic Cardiomyopathy Is Mitigated By H 2 S Diabetes Is Amentioning

confidence: 99%

Emerging role of hydrogen sulfide-microRNA crosstalk in cardiovascular diseases

Hackfort

Mishra

2016

American Journal of Physiology-Heart and Circulatory Physiology

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Hydrogen sulfide upregulates KATP channel expression in vascular smooth muscle cells of spontaneously hypertensive rats

Cited by 60 publications

References 44 publications

Impaired Hydrogen Sulfide–Mediated Vasodilation Contributes to Microvascular Endothelial Dysfunction in Hypertensive Adults

Impaired Hydrogen Sulfide–Mediated Vasodilation Contributes to Microvascular Endothelial Dysfunction in Hypertensive Adults

The role of hydrogen sulfide in aging and age-related pathologies

Emerging role of hydrogen sulfide-microRNA crosstalk in cardiovascular diseases

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