title: Antioxidant treatment prevents renal damage and dysfunction and reduces arterial pressure in salt-sensitive hypertension.
abstract: The goal of this study was to test the hypothesis that oxidative stress in Dahl salt-sensitive (SS) rats on a high-sodium intake contributes to the progression of renal damage, the decreases in renal hemodynamics, and the development of hypertension. We specifically studied whether antioxidant therapy, using vitamins C and E, could help prevent renal damage and glomerular filtration rate (GFR) and renal plasma flow reductions and attenuate the increases in arterial pressure. Thirty-three 7- to 8-week old Dahl SS/Rapp strain rats were placed on either a high-sodium (8%) or a low-sodium (0.3%) diet with or without vitamin E (111 IU/d) in the food and 98 mg/d vitamin C in the drinking water for 5 weeks. Rats were equipped with indwelling arterial and venous catheters at day 21. By day 35 in the rats with high-sodium diet, vitamin C and E treatment significantly decreased renal cortical and medullary O2*- release, mean arterial pressure, urinary protein excretion, glomerular necrosis, and renal tubulointerstitial damage. At this time, GFR significantly decreased in the high-sodium diet group (1.6+/-0.2 mL/min) when compared with either the high-sodium plus vitamins C and E (2.9+/-0.2 mL/min) or the low-sodium diet group (2.9+/-0.3 mL/min). In SS rats on high-sodium diet, renal plasma flow decreased 40%, and this reduced flow was restored by vitamin treatment. In Dahl salt-sensitive hypertension, increased oxidative stress plays an important role in the renal damage, decreases in renal hemodynamics, and increases in arterial pressure that occur. Antioxidant treatment with vitamins C and E improves renal dysfunction, lessens renal injury, and decreases arterial pressure in Dahl salt-sensitive hypertension.
authors.affiliation: Department of Physiology and Biophysics, University of Mississippi Medical Center, Jackson, USA.
authors.forename: Niu
authors.initials: N
authors.lastname: Tian
authors.forename: Kristina D
authors.initials: KD
authors.lastname: Thrasher
authors.forename: Paul D
authors.initials: PD
authors.lastname: Gundy
authors.forename: Michael D
authors.initials: MD
authors.lastname: Hughson
authors.forename: R Davis
authors.initials: RD
authors.lastname: Manning
mesh_terms: D000818:Animals; D000975:Antioxidants / Q000627:therapeutic use*; D001205:Ascorbic Acid / Q000627:therapeutic use; D001794:Blood Pressure / Q000187:drug effects*; D006339:Heart Rate / Q000187:drug effects; D006439:Hemodynamics / Q000187:drug effects; D006973:Hypertension / Q000139:chemically induced* / Q000188:drug therapy* / Q000473:pathology / Q000503:physiopathology; D007668:Kidney / Q000473:pathology; D007672:Kidney Cortex / Q000378:metabolism; D007674:Kidney Diseases / Q000517:prevention & control*; D007679:Kidney Medulla / Q000378:metabolism; D008297:Male; D011507:Proteinuria / Q000503:physiopathology; D051381:Rats; D020303:Rats, Inbred Dahl; D012079:Renal Circulation / Q000187:drug effects; D012965:Sodium Chloride; D013481:Superoxides / Q000378:metabolism; D014810:Vitamin E / Q000627:therapeutic use
chemical_list: D000975:Antioxidants; D013481:Superoxides; D014810:Vitamin E; D012965:Sodium Chloride; D001205:Ascorbic Acid