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Endothelin-1-induced contraction in veins is independent of hydrogen peroxide

Department of Pharmacology and Toxicology, Michigan State University, East Lansing, Michigan

Submitted 28 January 2005 ; accepted in final form 16 May 2005

Reactive oxygen species (ROS), such as superoxide and H₂O₂, are capable of modifying vascular tone, although the response to ROS can vary qualitatively among vascular beds, experimental procedures, and species. Endothelin-1 (ET-1) induces superoxide production, which can be dismutated to H₂O₂. The RhoA/Rho kinase pathway partially mediates ET-1-induced contraction and recently was implicated in superoxide-induced contraction. We hypothesized that H₂O₂, not superoxide, mediates venous ET-1-induced contraction. Rat thoracic aorta and vena cava contracted to exogenously added H₂O₂ (1 µM–1 mM) [maximum aortic contraction = 10 ± 3% of phenylephrine (10 µM) contraction; maximum venous contraction = 85 ± 13% of norepinephrine (10 µM) contraction]. (+)-(R)-trans-4-(1-aminoethyl-N-4-pyridil)cyclohexanecarboxamide dihydrochloride (Y-27632, 10 µM), a Rho kinase inhibitor, significantly reduced venous H₂O₂-induced contraction (15 ± 1% of control maximum) and reduced maximum ET-1-induced contraction by 59 ± 1%. However, neither the H₂O₂ scavenger catalase (100 and 2,000 U/ml) nor cell permeable polyethylene glycol-catalase (163 and 326 U/ml) reduced ET-1-induced contraction in the vena cava. The catalase inhibitor 3-aminotriazole (3-AT) also had no effect on maximal venous ET-1-induced contraction. Basal H₂O₂ levels were three times higher in the vena cava than in the aorta (vena cava, 0.74 ± 0.09 nmol H₂O₂/mg protein; aorta, 0.24 ± 0.05 nmol H₂O₂/mg protein). ET-1 (100 nM) increased H₂O₂ in the vena cava but not in the aorta (vena cava, 154.10 ± 17.29% of control H₂O₂; aorta, 83.72 ± 20.20%). Antagonism of either ET_A or ET_B receptors with the use of atrasentan (30 nM) or BQ-788 (100 nM), respectively, reduced ET-1 (100 nM)-induced increases in venous H₂O₂. In summary, ET-1 increased H₂O₂ in veins but not arteries, and venous ET-1-induced H₂O₂ production was independent of the contractile properties of ET-1.

venous contractility; reactive oxygen species

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