Olmesartan Ameliorates Renovascular Injury and Oxidative Stress in Zucker Obese Rats Enhanced by Dietary Protein

The metabolic syndrome is a risk factor for the development of renal and vascular complications. Dietary protein intake aggravates renal injury in Zucker obese rats, a model of the metabolic syndrome. This study investigated whether dietary protein intake enhances renal and vascular injuries by oxid...

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Bibliographic Details
Published in:American journal of hypertension 2007-10, Vol.20 (10), p.1085-1091
Main Authors: Namikoshi, Tamehachi, Tomita, Naruya, Satoh, Minoru, Haruna, Yoshisuke, Kobayashi, Shinya, Komai, Norio, Sasaki, Tamaki, Kashihara, Naoki
Format: Article
Language:English
Subjects:
Aldehydes - metabolism
Angiotensin II Type 1 Receptor Blockers - pharmacology
Animals
Antihypertensive Agents - pharmacology
Arterial hypertension. Arterial hypotension
Biological and medical sciences
Blood and lymphatic vessels
Cardiology. Vascular system
Clinical manifestations. Epidemiology. Investigative techniques. Etiology
dietary protein
Dietary Proteins - adverse effects
Disease Models, Animal
Endothelium, Vascular - physiopathology
Experimental diseases
Hydralazine - pharmacology
Hypertension, Renovascular - chemically induced
Hypertension, Renovascular - physiopathology
Hypertension, Renovascular - prevention & control
Imidazoles - pharmacology
Kidney - metabolism
Male
Medical sciences
Metabolic syndrome
Metabolic Syndrome - etiology
Metabolic Syndrome - metabolism
Metabolic Syndrome - physiopathology
NADPH Oxidases - metabolism
Obesity - complications
Obesity - metabolism
Obesity - physiopathology
oxidative stress
Oxidative Stress - drug effects
Oxidative Stress - physiology
Rats
Rats, Zucker
renovascular injury
Tetrazoles - pharmacology
Zucker obese rats
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Summary:The metabolic syndrome is a risk factor for the development of renal and vascular complications. Dietary protein intake aggravates renal injury in Zucker obese rats, a model of the metabolic syndrome. This study investigated whether dietary protein intake enhances renal and vascular injuries by oxidative stress, and assessed effects of olmesartan, an angiotensin II type 1 receptor blocker, in this model. Zucker obese rats were fed either a standard protein diet, high protein diet (OHP), or high protein diet containing olmesartan or hydralazine for 12 weeks. We examined the glomerulosclerosis score, endothelium-dependent relaxation response in the aorta, 4-hydroxy-2-nonenal (HNE) contents in the kidney and aorta, and mRNA expression of NAD(P)H oxidase components (p22phox and p47phox) in the renal cortex. The OHP rats developed proteinuria, glomerulosclerosis, and endothelial dysfunction. Olmesartan prevented the development of all these damages in OHP rats, whereas hydralazine improved only glomerulosclerosis. The high protein diet also augmented HNE accumulation in glomeruli, renal arteries, and aortas, and increased the mRNA expressions of p22phox and p47phox in the renal cortex in obese rats. Olmesartan, but not hydralazine, inhibited all these changes. These results suggested that increased dietary protein intake exacerbates renal and vascular injuries, and augments oxidative stress in a rat model of the metabolic syndrome. Olmesartan ameliorated these injuries, presumably through its antioxidative effects, whereas hydralazine improved only glomerulosclerosis through its antihypertensive action. Dietary protein-enhanced injuries in the metabolic syndrome may be associated with hypercholesterolemia and the activated renin-angiotensin system.
ISSN:0895-7061
1879-1905
1941-7225
DOI:10.1016/j.amjhyper.2007.05.007