ArticleProceedings of the National Academy of Sciences of the United States of America2005
5-Methyltetrahydrofolate and tetrahydrobiopterin can modulate electrotonically mediated endothelium-dependent vascular relaxation.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 48 citations in OpenAlex.
- Folate administration decreases oxidative status and blood pressure in postmenopausal women.European journal of nutrition · 2015Trial
- Renal insulin-like growth factor binding-protein 7 is a critical promoter of progressive diabetic kidney disease.Nature communications · 2025Article
- Risk of Excess Maternal Folic Acid Supplementation in Offspring.Nutrients · 2024Review
- The Endothelium and COVID-19: An Increasingly Clear Link Brief Title: Endotheliopathy in COVID-19.International journal of molecular sciences · 2022Review
- Hypertension in chronic kidney disease: What lies behind the scene.Frontiers in pharmacology · 2022Review
- Uremic Toxins and Vascular Dysfunction.Toxins · 2020Review
- Endothelial control of vasodilation: integration of myoendothelial microdomain signalling and modulation by epoxyeicosatrienoic acids.Pflugers Archiv : European journal of physiology · 2014Review
- The effect of inorganic arsenic on endothelium-dependent relaxation: role of NADPH oxidase and hydrogen peroxide.Toxicology · 2013Article
- 2-Aminoethoxydiphenyl borate blocks electrical coupling and inhibits voltage-gated K+ channels in guinea pig arteriole cells.American journal of physiology. Heart and circulatory physiology · 2011Article
- Connexins and gap junctions in the EDHF phenomenon and conducted vasomotor responses.Pflugers Archiv : European journal of physiology · 2010Review
- Endothelial dysfunction in diabetes: multiple targets for treatment.Pflugers Archiv : European journal of physiology · 2010Review
- Hydrogen peroxide as an endothelium-derived hyperpolarizing factor.Pflugers Archiv : European journal of physiology · 2010Review
- Ascorbic acid and tetrahydrobiopterin potentiate the EDHF phenomenon by generating hydrogen peroxide.Cardiovascular research · 2009Article
- Endothelial injury induces vascular smooth muscle cell proliferation in highly localized regions of a direct contact co-culture system.Cell biochemistry and biophysics · 2008Article
Corrections and comments
- Erratum issued
Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
We have investigated the ability of 5-methyltetrahydrofolate (5-MTHF) and tetrahydrobiopterin (BH(4)) to modulate nitric oxide (NO)-independent vascular relaxations that are mediated by the sequential spread of endothelial hyperpolarization through the wall of the rabbit iliac artery by means of myoendothelial and homocellular smooth muscle gap junctions. Relaxations and subintimal smooth muscle hyperpolarizations evoked by cyclopiazonic acid were depressed by the gap junction inhibitor 2-aminoethoxydiphenyl borate, whose effects were prevented by 5-MTHF and BH(4), but not by their oxidized forms folic acid and 7,8-dihydrobiopterin. Analogously, 5-MTHF and BH(4), but not folic acid or 7,8-dihydrobiopterin, attenuated the depression of subintimal hyperpolarization by a connexin-mimetic peptide targeted against Cx37 and Cx40 ((37,40)Gap 26) and the depression of subadventitial hyperpolarization by a peptide targeted against Cx43 ((43)Gap 26), thus reflecting the known differential expression of Cx37 and Cx40 in the endothelium and Cx43 in the media of the rabbit iliac artery. The inhibitory effects of 2-aminoethoxydiphenyl borate and (37,40)Gap 26 against subintimal hyperpolarization were prevented by catalase, which destroys H(2)O(2). 5-MTHF and BH(4) thus appear capable of modulating electrotonic signaling by means of myoendothelial and smooth muscle gap junctions by reducing oxidant stress, potentially conferring an ability to reverse the endothelial dysfunction found in disease states through mechanisms that are independent of NO.
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