Hydrogen sulfide impairs shear stress-induced vasodilation in mouse coronary arteries
| العنوان: | Hydrogen sulfide impairs shear stress-induced vasodilation in mouse coronary arteries |
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| المؤلفون: | Qiang Chai, Hon Chi Lee, Tong Lu, Xaio Li Wang |
| المصدر: | Pflügers Archiv - European Journal of Physiology. 467:329-340 |
| بيانات النشر: | Springer Science and Business Media LLC, 2014. |
| سنة النشر: | 2014 |
| مصطلحات موضوعية: | BK channel, medicine.medical_specialty, Nitric Oxide Synthase Type III, Physiology, Clinical Biochemistry, Glycine, Hemodynamics, Vasodilation, Sulfides, Nitric Oxide, Mice, Enos, Physiology (medical), Internal medicine, Potassium Channel Blockers, Pressure, medicine, Animals, Hydrogen Sulfide, 4-Aminopyridine, Receptor, Cells, Cultured, biology, business.industry, Cystathionine gamma-Lyase, Endothelial Cells, Iberiotoxin, biology.organism_classification, Coronary Vessels, Coronary arteries, NG-Nitroarginine Methyl Ester, medicine.anatomical_structure, Endocrinology, Alkynes, Knockout mouse, biology.protein, Cardiology, Peptides, business |
| الوصف: | Hydrogen sulfide has emerged as an important endothelium-dependent vasodilator, but its role in shear stress-mediated dilation of coronary arteries is unclear. We examined the role of H2S on shear stress-mediated dilation of isolated mouse coronary arteries. In these vessels, Na2S produced concentration-dependent dilation, which was significantly inhibited by iberiotoxin and by 4-aminopyridine. In addition, BK and Kv currents in mouse coronary smooth muscle cells were directly activated by Na2S, suggesting that H2S produced vasodilation through BK and Kv channel activation. Using a pressure servo controller system, freshly isolated mouse coronary arteries were subjected to physiological levels of shear stress (1 to 25 dynes/cm(2)) and produced graded dilatory responses, but such effects were diminished in the presence of 100 μM Na2S. Pre-incubation with the cystathionine γ-lyase inhibitor, D,L-propargylglycine (PPG), resulted in a paradoxical augmentation of shear stress-mediated vasodilation. However, in the presence of L-NAME or in coronary arteries from eNOS knockout mice, PPG inhibited shear stress-mediated vasodilation, suggesting an interaction between NO and H2S signaling. Na2S inhibited eNOS activity in cultured mouse aortic endothelial cells and reduced the level of phospho-eNOS(serine 1177). These results suggest that both NO and H2S are important shear stress-mediated vasodilators in mouse coronary arteries but there is a complex interaction between these two signaling pathways that results in paradoxical vasoconstrictive effects of H2S through inhibition of NO generation. |
| تدمد: | 1432-2013 0031-6768 |
| URL الوصول: | https://explore.openaire.eu/search/publication?articleId=doi_dedup___::d63747ca4dd620062209a799d1e006fb https://doi.org/10.1007/s00424-014-1526-y |
| حقوق: | CLOSED |
| رقم الأكسشن: | edsair.doi.dedup.....d63747ca4dd620062209a799d1e006fb |
| قاعدة البيانات: | OpenAIRE |
Find this article in full text from Springer Verlag. | تدمد: | 14322013 00316768 |
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