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 . 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 of Hypertension – Wolters Kluwer Health
Published: Mar 1, 2018
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