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1 Department of Pharmacology and Toxicology, Michigan State University, East Lansing, MI, USA
* To whom correspondence should be addressed. E-mail: thakalik{at}msu.edu.
Reactive oxygen species (ROS), such as superoxide and hydrogen peroxide (H2O2), are capable of modifying vascular tone, though the response to ROS can vary qualitatively between 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]. 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 2000 U/ml) nor cell permeable PEG-catalase (163 and 326 U/ml) reduced ET-1-induced contraction in vena cava. The catalase inhibitor 3-aminotriazole (3-AT) also had no effect on maximal venous ET-1-induced contraction. Basal H2O2 levels were 3 times higher in vena cava than aorta (vena cava: 0.74±0.09 nmol H2O2/mg protein; aorta: 0.24±0.05). ET-1 (100 nM) increased H2O2 in vena cava but not aorta (vena cava: 154.10±17.29% of control H2O2; aorta: 83.72±20.20%). Antagonism of either ETA or ETB receptors using 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.
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