title: Heat shock augments angiotensin II-induced vascular contraction through increased production of reactive oxygen species.
abstract: A temporal increase in temperature triggers a series of stress responses and alters vascular smooth muscle (VSM) contraction induced by agonist stimulation. Here we examined the role of reactive oxygen species (ROS) in heat shock-dependent augmentation of angiotensin II (AngII)-induced VSM contraction. Endothelium-denuded rat aortic rings were treated with heat shock for 45 min at 42 degrees C and then subjected to assays for the production of force, ROS, and the expression of ROS-related enzymes. AngII-induced contraction was enhanced in heat shock-treated aorta. AngII-induced production of hydrogen peroxide and superoxide were elevated in response to the heat shock treatment. Pre-treatment with superoxide dismutases (SOD) mimetic and inhibitors for glutathione peroxidase and NADPH oxidase but not for xanthine oxidase eliminated an increase in the AngII-induced contraction in the heat shock-treated aorta. Heat shock increased the expression of p47phox, a cytosolic subunit of NADPH oxidase, but not Cu-Zn-SOD and Mn-SOD. In addition, heat shock increased contraction that was evoked by hydrogen peroxide and pyrogallol. These results suggest that heat shock causes an elevation of ROS as well as a sensitization of ROS signal resulting in an augmentation of VSM contraction in response to agonist.
authors.affiliation: Department of Pharmacology and Cardiovascular Research Institute, Kyungpook National University School of Medicine, Daegu 700-422, Republic of Korea.
authors.forename: Jee In
authors.initials: JI
authors.lastname: Kim
authors.forename: Sang Won
authors.initials: SW
authors.lastname: Jung
authors.forename: Enyue
authors.initials: E
authors.lastname: Yang
authors.forename: Kwon Moo
authors.initials: KM
authors.lastname: Park
authors.forename: Masumi
authors.initials: M
authors.lastname: Eto
authors.forename: In Kyeom
authors.initials: IK
authors.lastname: Kim
mesh_terms: D000804:Angiotensin II / Q000494:pharmacology; D000818:Animals; D001011:Aorta / Q000187:drug effects / Q000502:physiology; D018869:Heat-Shock Response; D009131:Muscle, Smooth, Vascular / Q000187:drug effects / Q000502:physiology*; D009249:NADP / Q000096:biosynthesis; D019255:NADPH Oxidases / Q000096:biosynthesis; D051381:Rats; D017382:Reactive Oxygen Species / Q000378:metabolism*; D013482:Superoxide Dismutase / Q000096:biosynthesis; D014661:Vasoconstriction
chemical_list: D017382:Reactive Oxygen Species; D000804:Angiotensin II; D009249:NADP; D013482:Superoxide Dismutase; D019255:NADPH Oxidases; C060505:neutrophil cytosolic factor 1