ArticleCirculation research2010
Increased endothelial exocytosis and generation of endothelin-1 contributes to constriction of aged arteries.
Article in Circulation research, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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Who cites it
30 citing papers in PubMed, 62 citations in OpenAlex.
- Oral sapropterin augments reflex vasoconstriction in aged human skin through noradrenergic mechanisms.Journal of applied physiology (Bethesda, Md. : 1985) · 2013Trial
- Endothelin-1 in Health and Disease.International journal of molecular sciences · 2023Review
- Vascular aging and cardiovascular disease: pathophysiology and measurement in the coronary arteries.Frontiers in cardiovascular medicine · 2023Review
- ET-1 as a Sex-Specific Mechanism Impacting Age-Related Changes in Vascular Function.Frontiers in aging · 2021Review
- Altered Vascular Adaptations to Pregnancy in a Rat Model of Advanced Maternal Age.Frontiers in physiology · 2021Article
- The clinical effects of l-arginine and asymmetric dimethylarginine: implications for treatment in secondary Raynaud's phenomenon.Journal of the European Academy of Dermatology and Venereology : JEADV · 2019Review
- Proinflammatory Arterial Stiffness Syndrome: A Signature of Large Arterial Aging.Journal of vascular research · 2018Review
- Involvement of the metabolic sensor GPR81 in cardiovascular control.JCI insight · 2017Article
- Impaired activity of adherens junctions contributes to endothelial dilator dysfunction in ageing rat arteries.The Journal of physiology · 2017Article
- Gasotransmitter Heterocellular Signaling.Antioxidants & redox signaling · 2017Article
- In Development-A New Paradigm for Understanding Vascular Disease.Journal of cardiovascular pharmacology · 2017Review
- Aging-related alterations in eNOS and nNOS responsiveness and smooth muscle reactivity of murine basilar arteries are modulated by apocynin and phosphorylation of myosin phosphatase targeting subunit-1.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2017Article
- Now you see it, now you don't: the changing face of endothelin-1 signalling during vascular ontogenesis.The Journal of physiology · 2016Article
- Local renin-angiotensin system mediates endothelial dilator dysfunction in aging arteries.American journal of physiology. Heart and circulatory physiology · 2016Article
- Immature endothelial cells initiate endothelin-mediated constriction of newborn arteries.The Journal of physiology · 2016Article
- N-ethylmaleimide‑sensitive factor siRNA inhibits the release of Weibel-Palade bodies in endothelial cells.Molecular medicine reports · 2016Article
- Advanced glycation end products upregulate lysyl oxidase and endothelin-1 in human aortic endothelial cells via parallel activation of ERK1/2-NF-κB and JNK-AP-1 signaling pathways.Cellular and molecular life sciences : CMLS · 2016Article
- N-Ethylmaleimide Sensitive Factor (NSF) Inhibition Prevents Vascular Instability following Gram-Positive Pulmonary Challenge.PloS one · 2016Article
- Inverse Correlation Between Plasma Adropin and ET-1 Levels in Essential Hypertension: A Cross-Sectional Study.Medicine · 2015Observational
- A vascular mechanistic approach to understanding Raynaud phenomenon.Nature reviews. Rheumatology · 2015Review
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
rationaleCirculating levels of endothelin (ET)-1 and endogenous ET(A)-mediated constriction are increased in human aging. The mechanisms responsible are not known.
objectiveInvestigate the storage, release, and activity of ET-1 system in arteries from young and aged Fischer-344 rats. METHODS AND
resultsAfter NO synthase inhibition (L-NAME), thrombin contracted aged arteries, which was inhibited by endothelial denudation, ET(A) receptor antagonism (BQ123), and ECE inhibition (phosphoramidon, SM19712) or by inhibiting exocytosis (TAT-NSF, N-ethylmaleimide-sensitive factor inhibitor). Thrombin did not cause endothelium-dependent contraction of young arteries. In aged but not young arteries, thrombin rapidly increased ET-1 release, which was abolished by endothelium denudation or TAT-NSF. L-NAME did not affect ET-1 release. ET-1 immunofluorescent staining was punctate and distinct from von Willebrand factor (VWF). VWF and ET-1 immunofluorescent intensity was similar in young and aged quiescent arteries. Thrombin rapidly increased ET-1 staining and decreased VWF staining in aged but had no effect in young aortas. After L-NAME, thrombin decreased VWF staining in young aortas. NO donor DEA-NONOate (1 to 100 nmol/L) reversed thrombin-induced exocytosis in young (VWF) but not aged L-NAME-treated aortas (VWF, ET-1). Expression of preproET-1 mRNA and ECE-1 mRNA were increased in aged compared to young endothelium. BigET-1 levels and contraction to exogenous BigET-1 (but not ET-1) were also increased in aged compared to young arteries.
conclusionsThe stimulated exocytotic release of ET-1 is dramatically increased in aged endothelium. This reflects increased reactivity of exocytosis, increased expression and storage of ET-1 precursor peptides, and increased expression of ECE-1. Altered endothelial exocytosis of ET-1 and other mediators may contribute to cardiovascular pathology in aging.
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