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Arterial stiffness and hypertension in diet‐induced obese mice
Author(s) -
Seta Francesca,
Shiang Tina,
Weisbrod Robert,
Chauhan Pratibha,
Bajpai Saumendra,
Reinhart-King Cynthia,
Cohen Richard
Publication year - 2012
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.26.1_supplement.lb531
Subject(s) - arterial stiffness , medicine , pulse wave velocity , endocrinology , blood pressure , aorta , cardiology , basal (medicine) , diabetes mellitus , renin–angiotensin system , pulse pressure , insulin resistance , obesity
BACKGROUND Arterial stiffness (AS) may contribute to increased blood pressure (BP) during aging and obesity and is an independent predictor of cardiovascular complications. AIMS To elucidate the molecular mechanisms of arterial stiffness and its relationship to the development of hypertension in a model of diet‐induced obesity. METHODS AND RESULTS C57BL/6J mice fed high fat‐high sucrose diet (HFHS), showed increased fat mass, body weight and insulin resistance compared to normal diet (ND). Pulse wave velocity (PWV), the speed of pressure waveform propagation along the aorta used as index of AS, increased by 2.5‐fold after 2 mos HFHS and remained elevated thereafter while BP, measured by radiotelemetry, increased only after 8 mos HFHS. Microalbuminuria, an index of renal dysfunction, developed after 4 mos HFHS. Aortic wall thickness and renin increased after 2 mos HFHS suggesting that renin‐angiotensin‐aldosterone system (RAAS) may contribute to AS in advance of hypertension. Stiffness modulus of aortic extracellular basal membrane, determined in vitro, was increased at 8 mos HFHS. CONCLUSIONS In diet‐induced obese mice, AS precedes the development of hypertension and kidney dysfunction. Our results suggest that RAAS may contribute to structural changes in aortic smooth muscle, as evidenced by aortic wall thickening and extracellular basal membrane stiffening, causing AS.