title: Hydrogen peroxide emerges as a regulator of tone in skeletal muscle arterioles during juvenile growth.
abstract: 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 (H2O2) 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 H2O2 formation, and arteriolar dilation to exogenous H2O2 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 H2O2 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 H2O2 contributes to endothelium-dependent arteriolar dilation in juvenile rats, but not in younger rats, and that H2O2 acts in juvenile rats by stimulating endothelial NO release and activating smooth muscle K+ channels.
authors.affiliation: Department of Physiology and Pharmacology, West Virginia University School of Medicine, Morgantown, WV 26505-9105, USA.
authors.forename: Julie Balch
authors.initials: JB
authors.lastname: Samora
authors.forename: Jefferson C
authors.initials: JC
authors.lastname: Frisbee
authors.forename: Matthew A
authors.initials: MA
authors.lastname: Boegehold
mesh_terms: D000109:Acetylcholine / Q000494:pharmacology; D000818:Animals; D000924:Anticholesteremic Agents / Q000494:pharmacology; D000975:Antioxidants / Q000494:pharmacology; D001160:Arterioles / Q000254:growth & development; D002374:Catalase / Q000494:pharmacology; D004730:Endothelium, Vascular / Q000254:growth & development* / Q000378:metabolism; D006861:Hydrogen Peroxide / Q000378:metabolism* / Q000494:pharmacology; D008297:Male; D009129:Muscle Tonus / Q000187:drug effects / Q000502:physiology*; D018482:Muscle, Skeletal / Q000098:blood supply* / Q000254:growth & development*; D009131:Muscle, Smooth, Vascular / Q000254:growth & development; D052247:Nitric Oxide Synthase Type II / Q000378:metabolism; D052250:Nitric Oxide Synthase Type III; D016877:Oxidants / Q000494:pharmacology; D026902:Potassium Channel Blockers / Q000494:pharmacology; D015221:Potassium Channels / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D019821:Simvastatin / Q000494:pharmacology; D014664:Vasodilation / Q000187:drug effects / Q000502:physiology*; D014665:Vasodilator Agents / Q000494:pharmacology
chemical_list: D000924:Anticholesteremic Agents; D000975:Antioxidants; D016877:Oxidants; D026902:Potassium Channel Blockers; D015221:Potassium Channels; D014665:Vasodilator Agents; D019821:Simvastatin; D006861:Hydrogen Peroxide; D002374:Catalase; D052247:Nitric Oxide Synthase Type II; D052250:Nitric Oxide Synthase Type III; C496316:Nos3 protein, rat; D000109:Acetylcholine