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J Am Soc Nephrol 14:2783-2789, 2003
© 2003 American Society of Nephrology

BASIC SCIENCE

Role of Oxidative Stress in Endothelial Dysfunction and Enhanced Responses to Angiotensin II of Afferent Arterioles from Rabbits Infused with Angiotensin II

Dan Wang, Yifan Chen, Tina Chabrashvili, Shakil Aslam, Lillian J. Borrego Conde, Jason G. Umans and Christopher S. Wilcox

Division of Nephrology and Hypertension and Center for Hypertension and Renal Disease Research, Georgetown University, Washington, DC

Correspondence to Dr. Christopher S. Wilcox, Division of Nephrology and Hypertension, Georgetown University Medical Center, 3800 Reservoir Road, NW, PHC F6003, Washington, DC 20007. Phone: 202-687-9183; Fax: 202-687-7893;

ABSTRACT. The hypothesis that O2·- enhances angiotensin II (AngII)-induced vasoconstriction and impairs acetylcholine-induced vasodilation of afferent arterioles (Aff) in AngII–induced hypertension was investigated. Rabbits (n = 6 per group) received 12 to 14 d of 0.154 M NaCl (Sham), subpressor AngII (60 ng/kg per min; AngII 60) or slow pressor AngII (200 ng/kg per min; AngII 200). Individual Aff were perfused in vitro at 60 mmHg. AngII 200 increased mean arterial pressure (mean ± SD; 103 ± 9 versus 73 ± 6 mmHg; P < 0.01), plasma lipid peroxides (2.6 ± 0.3 versus 2.0 ± 0.3 nM; P < 0.05), renal cortical NADPH- and NADH-dependent O2·- generation, and Aff mRNA for p22phox 5-fold (P < 0.001) but decreased that for AT1-receptor 2.4-fold (P < 0.01). AngII 60 increased only NADH-dependent O2·- generation by renal cortex. Aff from AngII 200 rabbits had diminished acetylcholine relaxations (+50 ± 4 versus +85 ± 6%; P < 0.001), but these became similar in the presence of nitro-L-arginine (10-4 M). Aff from AngII 60 and AngII 200 rabbits had unchanged norepinephrine contractions (10-7 M) but significantly (P < 0.05) enhanced AngII contractions (10-8 M: Sham -52 ± 5 versus AngII 60 to 77 ± 5 versus AngII 200 to 110 ± 10%). The superoxide dismutase mimetic tempol (10-4 M) moderated the AngII responses of Aff from AngII 200 rabbits to levels of AngII 60 rabbits (-64 ± 7%). The AngII slow pressor response enhances renal cortical O2·- and p22phox expression. Increased O2·- generation in Aff mediates an impaired nitric oxide synthase–dependent endothelium-derived relaxing factor response and paradoxically enhances contractions to AngII despite downregulation of the mRNA for AT1 receptors. A subpressor dose of AngII enhances Aff responses to AngII independent of O2·-. E-mail: wilcoxch@georgetown.edu




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