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Hydrogen Peroxide Emerges as a Regulator of Tone in Skeletal Muscle Arterioles During Juvenile Growth
Author(s) -
Samora Julie Balch,
Frisbee Jefferson C.,
Boegehold Matthew A.
Publication year - 2008
Publication title -
microcirculation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.793
H-Index - 83
eISSN - 1549-8719
pISSN - 1073-9688
DOI - 10.1080/10739680701508497
Subject(s) - catalase , endocrinology , medicine , skeletal muscle , arteriole , chemistry , vasodilation , weanling , endothelium , juvenile , acetylcholine , endogeny , biology , anatomy , circulatory system , oxidative stress , genetics
Objective: The endothelium‐dependent dilation of skeletal muscle arterioles is mediated by factors that have not been identified in young rats, and partly mediated by an unidentified hyperpolarizing factor in maturing rats. This study was designed to determine if endogenous hydrogen peroxide (H 2 O 2 ) contributes to this arteriolar dilation at either of these growth stages. Methods: Gracilis muscle arterioles were isolated from rats at ages 24–26 days (“weanlings”) and 46–48 days (“juveniles”). We investigated the effects of catalase treatment on the endothelium‐dependent dilation of these vessels to simvastatin and acetylcholine (ACh). Catalase‐sensitive 2′,7′‐dichlorofluorescein (DCF) fluorescence also was measured as an index of H 2 O 2 formation, and arteriolar dilation to exogenous H 2 O 2 was pharmacologically probed in each age group. Results: Responses to simvastatin and ACh were attenuated by catalase in juvenile, but not weanling, arterioles. Juvenile, but not weanling, arterioles also displayed catalase‐sensitive DCF fluorescence that was increased by ACh. Exogenous H 2 O 2 could induce dilation in juvenile, but not weanling, arterioles. In juvenile arterioles, this dilation was abolished by the K + channel inhibitors TEA and glibenclamide, and attenuated by NOS inhibition or endothelial removal. Conclusions: These findings suggest that endogenous H 2 O 2 contributes to endothelium‐dependent arteriolar dilation in juvenile rats, but not in younger rats, and that H 2 O 2 acts in juvenile rats by stimulating endothelial NO release and activating smooth muscle K + channels.