title: Obesity-induced hypertension develops in young rats independently of the renin-angiotensin-aldosterone system.
abstract: A correlation exists between obesity and hypertension. In the currently available models of diet-induced obesity, the treatment of rats with a high fat (HF) diet does not begin until adulthood. Our aim was to develop and characterize a model of pre-pubescent obesity-induced hypertension. Male Sprague-Dawley rats were fed a HF diet (35% fat) for 10 weeks, beginning at age 3 weeks. Blood pressure was measured by tail-cuff, and a terminal blood sample was obtained to measure fasting blood glucose, insulin, plasma renin, aldosterone, thiobarbitutic acid reactive substances (TBARS), and free 8-isoprostanes levels. The vascular reactivity in the aorta was assessed using a myograph. Blood pressure was increased in rats fed the HF diet (HF, 161 +/- 2 mm Hg vs. control, 137 +/- 2 mm Hg, P < 0.05). Blood glucose (HF, 155 +/- 4 mg/dL vs. control, 123 +/- 5 mg/dL, P < 0.05), insulin (HF, 232 +/- 63 pM vs. control, 60 +/- 11 pM, P < 0.05), TBARS (expressed as nM of malondialdehyde [MDA]/ml [HF, 1.8 +/- 0.37 nM MDA/ml vs. control 1.05 +/- 0.09 nM MDA/ml, P < 0.05]), and free 8-isoprostanes (HF, 229 +/- 68 pg/ml vs. control, 112 +/- 9 pg/ml, P < 0.05) levels were elevated in the HF diet group. Interestingly, plasma renin and aldosterone levels were not different between the groups. The maximum vasoconstriction to phenylephrine (10(-4) M) was increased in the HF diet group (HF, 26.1 +/- 1.5 mN vs. control 22.3 +/- 1.2 mN, P < 0.05). In conclusion, pre-pubescent rats become hypertensive and have increased oxidative stress and enhanced vasoconstriction when fed a HF diet. Surprisingly, this occurs without the increase in renin or aldosterone levels seen in the adult models of diet-induced obesity.
authors.affiliation: Department of Physiology, Medical College of Georgia, Augusta, 30912-3000, USA. asmithgs@students.mcg.edu
authors.forename: Anita D
authors.initials: AD
authors.lastname: Smith
authors.forename: Michael W
authors.initials: MW
authors.lastname: Brands
authors.forename: Mong-Heng
authors.initials: MH
authors.lastname: Wang
authors.forename: Anne M
authors.initials: AM
authors.lastname: Dorrance
mesh_terms: D000109:Acetylcholine / Q000494:pharmacology; D000375:Aging / Q000097:blood; D000450:Aldosterone / Q000097:blood; D000818:Animals; D001786:Blood Glucose; D002319:Cardiovascular System / Q000187:drug effects / Q000503:physiopathology*; D004041:Dietary Fats / Q000008:administration & dosage; D004195:Disease Models, Animal; D006321:Heart / Q000033:anatomy & histology; D006973:Hypertension / Q000209:etiology* / Q000503:physiopathology*; D007328:Insulin / Q000097:blood; D050152:Intra-Abdominal Fat / Q000473:pathology; D008297:Male; D009765:Obesity / Q000503:physiopathology*; D009929:Organ Size; D018384:Oxidative Stress; D010656:Phenylephrine / Q000494:pharmacology; D051381:Rats; D017207:Rats, Sprague-Dawley; D012083:Renin / Q000097:blood; D012084:Renin-Angiotensin System / Q000502:physiology*; D017392:Thiobarbituric Acid Reactive Substances / Q000032:analysis; D014661:Vasoconstriction / Q000187:drug effects
chemical_list: D001786:Blood Glucose; D004041:Dietary Fats; D007328:Insulin; D017392:Thiobarbituric Acid Reactive Substances; D010656:Phenylephrine; D000450:Aldosterone; D012083:Renin; D000109:Acetylcholine