Homocysteine induces endothelial dysfunction via inhibition of arginine transport.

Homocysteine induces endothelial dysfunction via inhibition of arginine transport. Research Abstract Details 

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Homocysteine induces endothelial dysfunction via inhibition of arginine transport. Abstract Text:

L Jin,R B Caldwell,T Li-Masters,R W Caldwell,

Hyperhomocysteinemia is an independent risk factor for cardiovascular diseases. High levels of plasma homocysteine (HCY) increase oxidative stress and reduce endothelial-dependent relaxation. We determined whether hyperhomocysteinemia-induced endothelial dysfunction is mediated through inhibition of cellular transport of L-arginine. In endothelial cells, HCY had a biphasic effect on arginine transport. HCY treatment for 6 hr increased L-arginine uptake by 34%; however, uptake was decreased by 25% after 24 h. HCY caused membrane hyperpolarization during both 6 and 24 h incubation periods, indicating that the negative charge facilitating arginine uptake was maintained. HCY significantly reduced expression of cellular arginine transporter protein (CAT-1) after 24 h treatment; whereas endothelial nitric oxide synthase (eNOS) protein levels and basal eNOS activity were not altered. Nevertheless, nitric oxide (NO) formation was significantly decreased. The antioxidant ascorbic acid prevented the effect of HCY on arginine transport. HCY induced formation of the peroxynitrite biomarker nitrotyrosine, which was blocked by supplemental L-arginine. HCY treatment of aortic rings caused decreased vasorelaxation to acetylcholine, which was prevented by supplemental arginine. In conclusion, HCY decreased NO formation and induced endothelial dysfunction without altering protein level or basal activity of eNOS, but through decreases in function and protein expression of the CAT-1 transporter. Reduced arginine supply may lead to eNOS uncoupling and generation of superoxide, contributing to HCY-induced oxidative stress.

Homocysteine induces endothelial dysfunction via inhibition of arginine transport. Publishing Authors By Initials

L Jin,RB Caldwell,T Li-Masters,RW Caldwell,

For similar vasodilation research abstracts see: vasodilation research

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Homocysteine induces endothelial dysfunction via inhibition of arginine transport. Journal Published:

PUBLICATION TYPE: Research Support, Non-U.S. Gov

Journal: Journal of physiology and pharmacology : an offici

VOLUME: 58

Page Numbers: 191-206

Journal Abbreviation: J. Physiol. Pharmacol.

ISSN: 0867-5910

DAY: 3

MONTH: Jun

YEAR: 2007

Homocysteine induces endothelial dysfunction via inhibition of arginine transport. Information

Number of References:

LANGUAGE: eng

NlmUniqueID: 9114501

Homocysteine induces endothelial dysfunction via inhibition of arginine transport. Keywords Mesh Terms:

KEYWORDS: Vasodilation

MESH TERMS: drug effects

Chemical & Substance for Abstract: Homocysteine induces endothelial dysfunction via inhibition of arginine transport. Information

Substance Name: Nitric Oxide Synthase Type III

Registry Number: EC 1.14.13.39

Grant and Affiliation Information for Homocysteine induces endothelial dysfunction via inhibition of arginine transport.

AFFILIATION: Department of Pharmacology and Toxicology, Medical College of Georgia, Augusta, Georgia 30912, USA.

Country: Poland

AGENCY: United States NHLBI

GRANT: NIH-HL070215

ACRONYM: HL

MEDLINETA: J Physiol Pharmacol

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