Oxidative stress and antioxidant treatment in hypertension and the associated renal damage.
Reactive oxygen species (ROS) are elevated in humans with hypertension many of which develop end-stage renal disease (ESRD), and antioxidant capacity is decreased. About one-half of essential hypertensives have a salt-sensitive type of hypertension, and the amount of renal damage that occurs in salt-sensitive hypertensives greatly exceeds that of non-salt-sensitive hypertensives. Antioxidant therapy can improve cardiovascular outcomes in humans but only if sufficient doses are used. Salt-sensitive hypertensive animal models, especially Dahl salt-sensitive rats, have been used to investigate the relationship between hypertension, ROS and end-stage renal damage. In experimental salt-sensitive hypertension, ROS increase and significant renal damage occur. In the Dahl salt-sensitive (S) rat on high Na for 3 weeks, renal damage is mild, renal levels of superoxide dismutase are decreased, and treatment with Tempol reduces arterial pressure. In the Dahl S rat on high Na for 5 weeks, renal damage is severe, GFR and renal plasma flow are decreased, and renal superoxide production is high. Treatment with vitamins C and E decreases renal superoxide production and renal damage and prevents the decrease in renal hemodynamics. Antioxidant treatment reduces arterial pressure, aortic superoxide production and renal inflammation in DOCA-salt rats, and decreases blood pressure and aortic superoxide release and increases bioactive nitric oxide in SHR stroke-prone rats. In conclusion, in both human and experimental salt-sensitive hypertension, superoxide production and renal damage are increased, antioxidant capacity is decreased, and antioxidant therapy can be helpful.
Manning
R Davis
RD
Department of Physiology and Biophysics, University of Mississippi Medical Center Jackson, USA. dmanning@physiology.umsmed.edu
Tian
Niu
N
Meng
Shumei
S
D000818:Animals; D000975:Antioxidants / Q000627:therapeutic use*; D002318:Cardiovascular Diseases / Q000209:etiology / Q000503:physiopathology; D006801:Humans; D006973:Hypertension / Q000150:complications* / Q000503:physiopathology; D007676:Kidney Failure, Chronic / Q000209:etiology* / Q000503:physiopathology; D023421:Models, Animal; D018384:Oxidative Stress; D051381:Rats; D017382:Reactive Oxygen Species; D012492:Salts / Q000009:adverse effects; D012982:Sodium, Dietary / Q000009:adverse effects
D000975:Antioxidants; D017382:Reactive Oxygen Species; D012492:Salts; D012982:Sodium, Dietary