Published online before print July 28, 2003, doi: 10.1161/01.HYP.0000084853.47326.F2
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(Hypertension. 2003;42:316.)
© 2003 American Heart Association, Inc.
Scientific Contributions |
NADPH Oxidase–Derived Superoxide Augments Endothelin-1–Induced Venoconstriction in Mineralocorticoid Hypertension
From the Department of Pharmacology and Toxicology and the Neuroscience Program, Michigan State University, East Lansing, Mich.
Correspondence to Dr Alex F. Chen, Department of Pharmacology and Toxicology, B403 Life Sciences Bldg, Michigan State University, East Lansing, MI 48824-1317. E-mail chenal{at}msu.edu
Deoxycorticosterone acetate (DOCA)–salt hypertension is characterized by low renin/angiotensin but increased arterial superoxide levels. We have recently reported that the arterial endothelin-1 (ET-1) level is increased, resulting in NADPH oxidase activation and superoxide generation. However, the effect of ET-1 on venous superoxide production and its relation to venoconstriction are unknown. The present study tested the hypotheses that ET-1 stimulates venous NADPH oxidase and superoxide via its ETA receptors, resulting in enhanced venoconstriction in DOCA-salt hypertensive rats. Treatment with ET-1 (0.01 to 1 nmol/L), but not the selective ETB receptor agonist sarafotoxin s6c, of vena cavas of normal rats concentration-dependently increased superoxide levels, an effect that was abolished by the selective ETA receptor antagonist ABT-627. Although the ET-1 level was not increased in the vena cava and plasma, both venous NADPH oxidase activity and superoxide levels were significantly higher in DOCA-salt compared with sham rats. Moreover, ET-1 treatment (10-9 mol/L, 10 minutes) of isolated vena cavas further elevated superoxide levels in DOCA-salt rats only but not sham rats, an effect that was abrogated by the superoxide scavenger tempol. Similarly, ET-1–induced contractions of isolated vena cavas of DOCA-salt but not sham rats were significantly inhibited by tempol. The NADPH oxidase inhibitor apocynin significantly reduced superoxide levels in vena cavas of DOCA-salt rats and in ET-1–treated vena cavas of normal rats. Finally, in vivo ETA receptor blockade by ABT-627 significantly lowered venous superoxide levels and blood pressure in DOCA-salt but not sham rats. These results suggest that superoxide contributes to ET-1–induced venoconstriction through an elevated venous NADPH oxidase activity in mineralocorticoid hypertension.
Key Words: endothelin • venoconstriction • oxidative stress • hypertension, mineralocorticoid
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