Hydrogen sulfide, then nitric oxide and vasoprotection

Hydrogen sulfide, then nitric oxide and vasoprotection Editorial Comment Mark C. Chappell See original paper on page 651 ascular dysfunction is typically associated with experimental hypertension were associated with signifi- hypertension and contributes to the progression cantly lower levels of circulating H S [6]. In the human V of cardiovascular disease. Altered vascular tone that renal arteries, protein levels of the H S-generating enzyme constitutes an exaggerated vasoconstrictor response or an cystathionine g-lyase (CSE) were also lower in the hyper- attenuated ability for vasorelaxation may potentially lead to tensive vessels that appear to reflect an attenuated synthesis a chronic increase in vascular resistance and an elevation in of the enzyme. Moreover, H S exposure (12 h) of the blood pressure. A key component regulating vascular tone isolated renal arteries from the patients with hypertension is the nitric oxide (NO) system whereby activation of NO reversed the decline in CSE expression suggesting a posi- synthase (NOS) generates NO; the most prominent NOS tive feedback role of H S to maintain vascular synthesis. Of isoform in the vasculature is endothelial NOS (eNOS or NOS particular interest, H S exposure attenuated protein and type III) [1,2]. A well characterized signaling pathway for mRNA expression of the angiotensin-II type-1 receptor http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Journal of Hypertension Wolters Kluwer Health

Hydrogen sulfide, then nitric oxide and vasoprotection

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Publisher
Wolters Kluwer
Copyright
Copyright © 2018 Wolters Kluwer Health, Inc. All rights reserved.
ISSN
0263-6352
eISSN
1473-5598
D.O.I.
10.1097/HJH.0000000000001617
Publisher site
See Article on Publisher Site

Abstract

Editorial Comment Mark C. Chappell See original paper on page 651 ascular dysfunction is typically associated with experimental hypertension were associated with signifi- hypertension and contributes to the progression cantly lower levels of circulating H S [6]. In the human V of cardiovascular disease. Altered vascular tone that renal arteries, protein levels of the H S-generating enzyme constitutes an exaggerated vasoconstrictor response or an cystathionine g-lyase (CSE) were also lower in the hyper- attenuated ability for vasorelaxation may potentially lead to tensive vessels that appear to reflect an attenuated synthesis a chronic increase in vascular resistance and an elevation in of the enzyme. Moreover, H S exposure (12 h) of the blood pressure. A key component regulating vascular tone isolated renal arteries from the patients with hypertension is the nitric oxide (NO) system whereby activation of NO reversed the decline in CSE expression suggesting a posi- synthase (NOS) generates NO; the most prominent NOS tive feedback role of H S to maintain vascular synthesis. Of isoform in the vasculature is endothelial NOS (eNOS or NOS particular interest, H S exposure attenuated protein and type III) [1,2]. A well characterized signaling pathway for mRNA expression of the angiotensin-II type-1 receptor

Journal

Journal of HypertensionWolters Kluwer Health

Published: Mar 1, 2018

References

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