title: Effect of salt on hypertension and oxidative stress in a rat model of diet-induced obesity.
abstract: High-salt diet is known to induce or aggravate hypertension in animal models of hypertension and in humans. When Sprague-Dawley rats (n = 60) are fed a moderately high-fat diet (32% kcal fat, 0.8% NaCl) for 10 wk, about one-half develop obesity [obesity prone (OP)] and mild hypertension, whereas the other half [obesity resistant (OR)] maintain body weight equivalent to a low-fat control (C) and are normotensive. The aim of this study was to test the effect of high-NaCl diets (2 and 4% NaCl) on the development of hypertension and obesity, oxidative stress, and renal function. Both 2 and 4% NaCl induced an early increase in systolic blood pressure of OP but not OR or C rats. High-salt intake induced an increase in the size and reduction in number of adipocytes, concomitant to a twofold increase in circulating leptin in OP rats. Aortic superoxide generation indicated a 2.8-fold increase in the OP high-salt vs. normal-salt groups, whereas urine isoprostanes were not significantly increased. Also, hydroxynonenal protein adducts in the kidney were highly increased in OP rats on 2 and 4% NaCl, indicating oxidative stress in the renal tissue. Urine albumin was increased threefold in the OP on 2% NaCl and fourfold in the same group on 4% NaCl vs. 0.8% NaCl. Kidney histology indicated a higher degree of glomerulosclerosis in OP rats on high-salt diets. In summary, high-salt diet accelerated the development but did not increase the severity of hypertension; high salt increased oxidative stress in the vasculature and kidney and induced kidney glomerulosclerosis and microalbuminuria. Also, the OP rats on high salt displayed adipocyte hypertrophy and increased leptin production.
authors.affiliation: Department of Physiological Sciences, Eastern Virginia Medical School, 700W Olney Rd, Norfolk, VA 23507, USA. dobriaad@evms.edu
authors.forename: Anca D
authors.initials: AD
authors.lastname: Dobrian
authors.forename: Suzanne D
authors.initials: SD
authors.lastname: Schriver
authors.forename: Terrie
authors.initials: T
authors.lastname: Lynch
authors.forename: Russell L
authors.initials: RL
authors.lastname: Prewitt
mesh_terms: D017667:Adipocytes / Q000473:pathology; D000273:Adipose Tissue / Q000473:pathology; D000818:Animals; D001011:Aorta / Q000187:drug effects / Q000473:pathology; D001794:Blood Pressure / Q000187:drug effects; D001835:Body Weight / Q000187:drug effects; D004032:Diet / Q000009:adverse effects*; D004198:Disease Susceptibility; D004231:Diuresis / Q000187:drug effects; D006973:Hypertension / Q000209:etiology* / Q000503:physiopathology*; D006984:Hypertrophy; D007668:Kidney / Q000187:drug effects / Q000473:pathology; D020738:Leptin / Q000097:blood; D008297:Male; D009765:Obesity / Q000097:blood / Q000150:complications* / Q000209:etiology* / Q000473:pathology; D018384:Oxidative Stress / Q000187:drug effects*; D051381:Rats; D017207:Rats, Sprague-Dawley; D012083:Renin / Q000097:blood; D012598:Sclerosis; D017673:Sodium Chloride, Dietary / Q000008:administration & dosage*
chemical_list: D020738:Leptin; D017673:Sodium Chloride, Dietary; D012083:Renin