Effects of carotid baroreceptor stimulation on aortic remodeling in obese rats |
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Authors: | Qiao Yu Ling Shu Lang Wang Kaile Gao Jing Wang Mingyan Dai Quan Cao Yijie Zhang Qiang Luo Bangwang Hu Dilin Dai Jie Chen Mingwei Bao |
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Affiliation: | 1. Department of Cardiology, Renmin Hospital of Wuhan University, 238 Jiefang Road, Wuhan 430060, People''s Republic of China;2. Cardiovascular Research Institute, Wuhan University, Wuhan 430060, People''s Republic of China;3. Hubei Key Laboratory of Cardiology, Wuhan 430060, People''s Republic of China;4. Wuhan Ninth People''s Hospital, 20 Jilin Street, Qingshan District, Wuhan 430060, People''s Republic of China;5. Department of Cardiology, Suizhou Hospital, Hubei University of Medicine, Suizhou 441300, People''s Republic of China |
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Abstract: | Background and aimOur previous study found carotid baroreceptor stimulation (CBS) reduces body weight and white adipose tissue (WAT) weight, restores abnormal secretion of adipocytokines and inflammation factors, decreases systolic blood pressure (SBP) by inhibiting activation of sympathetic nervous system (SNS) and renin-angiotensin system (RAS) in obese rats. In this study, we explore effects of CBS on aortic remodeling in obese rats.Methods and resultsRats were fed high-fat diet (HFD) for 16 weeks to induce obesity and underwent either CBS device implantation and stimulation or sham operation at 8 weeks. BP and body weight were measured weekly. RAS activity of WAT, histological, biochemical and functional profiles of aortas were detected after 16 weeks. CBS effectively decreased BP in obese rats, downregulated mRNA expression of angiotensinogen (AGT) and renin in WAT, concentrations of AGT, renin, angiotensin II (Ang II), protein levels of Ang II receptor 1 (AT1R) and Ang II receptor 2 (AT2R) in WAT were declined. CBS inhibited reactive oxygen species (ROS) generation, inflammatory response and endoplasmic reticulum (ER) stress in aortas of obese rats, restrained vascular wall thickening and vascular smooth muscle cells (VSMCs) phenotypic switching, increased nitric oxide (NO) synthesis, promoted endothelium-dependent vasodilatation by decreasing protein expression of AT1R and leptin receptor (LepR), increasing protein expression of adiponectin receptor 1 (AdipoR1) in aortic VSMCs.ConclusionCBS reduced BP and reversed aortic remodeling in obese rats, the underlying mechanism might be related to the suppressed SNS activity, restored adipocytokine secretion and restrained RAS activity of WAT. |
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Keywords: | Carotid baroreceptor stimulation Renin-angiotensin system Aortic remodeling Obesity White adipose tissue |
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