on February 3, 2003
Circulation. 2003
Published online before print February 3, 2003, doi: 10.1161/01.CIR.0000051459.74466.46
Published online before print February 3, 2003, doi: 10.1161/01.CIR.0000051459.74466.46
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Submitted on September 26, 2002
From the Department of Pharmacology and Toxicology (L.L., G.D.F., S.W.W., C.A.N., J.J.G, A.F.C.) and the Neuroscience Program (G.D.F., J.J.G, A.F.C.), Michigan State University, East Lansing; and the Hypertension and Vascular Research Division (P.J.P.), Henry Ford Hospital, Detroit, Mich. * To whom correspondence should be addressed. E-mail: chenal{at}msu.edu.
Background--Angiotensin II-induced hypertension is associated with NAD(P)H oxidase-dependent superoxide production in the vessel wall. Vascular superoxide level is also increased in deoxycorticosterone acetate (DOCA)-salt hypertension, which is associated with a markedly depressed plasma renin activity because of sodium retention. However, the mechanisms underlying superoxide production in low-renin hypertension are undefined. Methods and Results--This study investigated (1) whether and how endothelin-1 (ET-1), which is increased in DOCA-salt hypertensive rats, contributes to arterial superoxide generation and (2) the effect of gene transfer of manganese superoxide dismutase and endothelial nitric oxide synthase. Both superoxide and ET-1 levels were significantly elevated in carotid arteries of DOCA-salt rats compared with that of the sham-operated controls. ET-1 concentration-dependently stimulated superoxide production in vitro in carotid arteries of normotensive rats. The increase in arterial superoxide in both ET-1-treated normotensive and DOCA-salt rats was reversed by a selective ETA receptor antagonist, ABT-627, the flavoprotein inhibitor diphenyleneiodonium, and the NADPH oxidase inhibitor apocynin but not by the nitric oxide synthase inhibitor N Conclusions--These findings suggest that ET-1 augments vascular superoxide production at least in part via an ETA/NADPH oxidase pathway in low-renin mineralocorticoid hypertension.
Revised on November 7, 2002
Accepted on November 8, 2002
Endothelin-1 Increases Vascular Superoxide via EndothelinA-NADPH Oxidase Pathway in Low-Renin Hypertension
Lixin Li MD,
-L-arginine methyl ester or the xanthine oxidase inhibitor allopurinol. Furthermore, in vivo blockade of ETA receptors significantly reduced arterial superoxide levels, with a concomitant decrease of systolic blood pressure in DOCA-salt rats. Ex vivo gene transfer of manganese superoxide dismutase or endothelial nitric oxide synthase also suppressed superoxide levels in carotid arteries of DOCA-salt rats.
Key words: endothelin • NADPH oxidase • superoxide • hypertension
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