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Cited by 26Nitric Oxide and Endothelin EffectsCardiovascular Health and Disease PreventionEicosanoids and Hypertension Pharmacology

The DOI matches its Crossref record; 54 of the 54 references it cites were found in a registry or an index.

Effects of Trientine, a Metal Chelator, on Defective Endothelium-dependent Relaxation in the Mesenteric Vasculature of Diabetic Rats

Inkster, Melanie E., Cotter, Mary A., Cameron, Norman E.·2002·Free Radical Research
DOI 10.1080/1071576021000028325
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Abstract

Diabetes mellitus compromises endothelium-dependent relaxation of blood vessels. This has been linked to the generation of reactive oxygen species (ROS), which neutralise nitric oxide (NO) and interfere with vasodilator function. Experiments using chelators have emphasised the importance of ROS produced by transition metal catalysed reactions. However, particularly for the small arteries and arterioles that control microcirculatory blood flow, NO is not the only endothelium-derived mediator; endothelium-derived hyperpolarizing factor (EDHF) has a major role. EDHF-mediated vasodilation is severely curtailed by diabetes; however, little information exists on the underlying pathophysiology. Deficits in the EDHF system, alone or in combination with the NO system, are crucial for the development of diabetic microvascular complications. To further elucidate the mechanisms involved, the aim was to examine the effects of diabetes and preventive and intervention chelator therapy with trientine on a preparation that has well-defined NO and EDHF-mediated responses, the rat mesenteric vascular bed. In phenylephrine-preconstricted preparations, maximum vasodilation to acetylcholine was reduced by 35 and 44% after 4 and 8 weeks of streptozotocin-induced diabetes, respectively. Trientine treatment over the first 4 weeks gave 72% protection; intervention therapy over the final 4 weeks prevented deterioration and corrected the initial deficit by 68%. These responses depend on both NO and EDHF. When the latter mechanism was isolated by NO synthase inhibition, diabetic deficits of 53.4 (4 weeks) and 65.4% (8 weeks) were revealed, that were 65% prevented and 50% corrected by trientine treatment. Neither diabetes nor trientine altered vascular smooth muscle responses to the NO donor, sodium nitroprusside (SNP). Thus, the data suggest that metal catalysed ROS production makes a substantial contribution to defects in both the EDHF and NO endothelial mechanisms in diabetes, which has therapeutic implications for microvascular complications.

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Crossref · 10.1080/1071576021000028325

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Metadata

Authors
Inkster, M. E., Cotter, M. A., & Cameron, N. E.
Affiliations
University of Aberdeen (GB)
ORCID
Venue
Free Radical Research
Publisher
Informa UK Limited
Published
2002-01
Volume
36
Issue
10
Pages
1091-1099
ISSN
  • 1029-2470 (ISSN-L)
  • 1071-5762
DOI
10.1080/1071576021000028325
OpenAlex
W1987191170
Cited by
26
References
54
Citations by year
2025: 1 · 2023: 1 · 2021: 1 · 2015: 3 · 2014: 1 · 2013: 1
FWCI
1.00
Type
journal article
Language
en
Open access
closed
Locations
  • Free Radical Research (publishedVersion)
  • PubMed (publishedVersion)
Topics
  • Health Sciences › Medicine › Physiology (medical) › Nitric Oxide and Endothelin Effects
  • Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiovascular Health and Disease Prevention
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Biochemistry › Eicosanoids and Hypertension Pharmacology
Keywords
triethylenetetramine, metal chelators, endothelium-dependent relaxation, diabetes mellitus, endothelium-derived hyperpolarizing factor, nitric oxide, reactive oxygen species, transition metal catalysis, mesenteric vasculature, streptozotocin-induced diabetes, acetylcholine, sodium nitroprusside, nitric oxide synthase, diabetic microvascular complications, vascular smooth muscle
MeSH terms
Acetylcholine, Animals, Biological Factors, Chelating Agents, Diabetes Mellitus, Experimental, Endothelium, Vascular, Enzyme Inhibitors, Male, Nitric Oxide, Nitroprusside, Phenylephrine, Splanchnic Circulation, Trientine, Vasoconstrictor Agents, Vasodilation, Rats, Sprague-Dawley, Nitric Oxide Synthase, Nitroarginine, Nitric Oxide Donors, Rats

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