| The activation of endothelin-1 pathway during methionine-induced homocysteinemia mediates endothelial dysfunction in hypertensive individuals. | |
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MedLine Citation:
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PMID: 20160653 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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OBJECTIVES: Endothelin-1 (ET-1) is a key regulator of arterial blood pressure in humans, and homocysteinemia is associated with increased oxidative stress. It is still unclear whether homocysteine-induced oxidative stress is implicated in the regulation of ET-1 expression. We examined the impact of acute homocysteinemia on endothelial function in hypertensive patients and healthy individuals, and the potential role of ET-1. METHODS: In this double-blind, placebo-controlled study, 39 hypertensive and 49 healthy individuals were randomized to receive high-dose vitamins (2 g vitamin C and 800IU vitamin E) or placebo followed by methionine loading 100 mg/kg body weight. Endothelium-dependent dilation (EDD) and endothelium-independent dilation (EID) of the brachial artery were evaluated by plethysmography, at baseline and 4 h postloading (4 h PML). ET-1 was measured by ELISA, whereas total lipid hydroperoxides (per-ox) levels were measured by a commercially available photometric technique. RESULTS: Acute, methionine-induced homocysteinemia decreased EDD in all study groups (P < 0.001 for all), whereas vitamins pretreatment failed to prevent this effect, despite the vitamins-induced reduction of peroxidation in the hypertensives group (P < 0.05). On the contrary, methionine loading significantly increased plasma ET-1 levels only in hypertensives (P < 0.05), an effect which was not prevented by antioxidant vitamins (P < 0.05). EID remained unchanged after methionine loading, in all study groups (P = NS for all groups). CONCLUSION: Experimental homocysteinemia rapidly blunts endothelial function in both hypertensive individuals and healthy individuals. The rapid elevation of ET-1 levels observed only in hypertensives, suggests that ET-1 may be the key mediator of homocysteine-induced endothelial dysfunction, independently of oxidative stress. |
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Authors:
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Dimitris Tousoulis; George Bouras; Charalambos Antoniades; Kyriakoula Marinou; Antigoni Miliou; Nikos Papageorgiou; George Chatzis; Costas Tentolouris; Costas Tsioufis; Christodoulos Stefanadis |
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Publication Detail:
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Type: Journal Article; Randomized Controlled Trial |
Journal Detail:
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Title: Journal of hypertension Volume: 28 ISSN: 1473-5598 ISO Abbreviation: J. Hypertens. Publication Date: 2010 May |
Date Detail:
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Created Date: 2010-04-16 Completed Date: 2010-07-29 Revised Date: - |
Medline Journal Info:
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Nlm Unique ID: 8306882 Medline TA: J Hypertens Country: England |
Other Details:
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Languages: eng Pagination: 925-30 Citation Subset: IM |
Affiliation:
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S Karagiorga 69, Glifada 166 75, Athens, Greece. drtousoulis@hotmail.com |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Adult Ascorbic Acid / administration & dosage Double-Blind Method Endothelin-1 / blood, physiology* Endothelium, Vascular / drug effects, physiopathology Female Homocysteine / blood* Humans Hyperhomocysteinemia / blood, etiology, physiopathology* Hypertension / blood, physiopathology* Male Methionine / administration & dosage* Oxidative Stress Signal Transduction Vasodilation / drug effects Vitamin E / administration & dosage |
| Chemical | |
Reg. No./Substance:
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0/Endothelin-1; 1406-18-4/Vitamin E; 454-28-4/Homocysteine; 50-81-7/Ascorbic Acid; 63-68-3/Methionine |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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