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Hydrogen Peroxide Mediates Endothelium‐Dependent Dilation of Coronary Arterioles in Obese Rats on a Low‐Carbohydrate Diet
Author(s) -
Focardi Marta,
Picchi Andrea,
Donnini Sandra,
Cameli Matteo,
Ziche Marina,
Marzilli Mario,
Mondillo Sergio
Publication year - 2013
Publication title -
microcirculation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.793
H-Index - 83
eISSN - 1549-8719
pISSN - 1073-9688
DOI - 10.1111/micc.12058
Subject(s) - vasodilation , catalase , endocrinology , sodium nitroprusside , medicine , nitric oxide , acetylcholine , endothelium , chemistry , endothelial dysfunction , hydrogen peroxide , oxidative stress , biochemistry
Objective Endothelium‐dependent vasodilation of coronary arterioles is impaired in obese rats and may be improved by a LCD. The aim of this study is to elucidate the mechanism by which this improvement occurs. Methods We used four groups of male Zucker rats: lean and obese on either SD or LCD. Coronary arterioles were cannulated and pressurized for diameter measurements during administration of acetylcholine or sodium nitroprusside or during flow. Real‐time PCR was performed to quantify mRNA expression of CuZnSOD and catalase. Results The LCD significantly increased endothelium‐dependent dilation in the obese rats. l ‐NAME and indomethacin reduced responses to flow and acetylcholine in the lean rats without any effect on the obese on either diet. In contrast, TEA and catalase blocked flow‐dependent and acetylcholine‐induced dilation in the obese on either diet, while no effect was observed on the lean. The LCD in the obese significantly up‐regulated catalase mRNA expression and slightly increased CuZnSOD mRNA levels. Conclusions A LCD improves endothelium‐dependent vasodilation of coronary arterioles in obese rats through the production of H 2 O 2 which acts as a hyperpolarizing factor, independent of nitric oxide and PGI 2 .