title: Arterial baroreflex dysfunction promotes atherosclerosis in rats.
abstract: The present study was designed to test the hypothesis that arterial baroreflex dysfunction promotes the development of atherosclerosis. Experiment 1: the baroreflex sensitivity (BRS) was measured in 30 Sprague-Dawley (SD) rats in conscious state with a computerized blood pressure monitoring system. Four weeks later, the rats were administered with Vitamin D3, and fed with the high-cholesterol diet for 8 weeks to induce atherosclerosis. The hearts and aortae were removed for pathological examination. A negative correlation was found between BRS and the scores of coronary (r=-0.464, P<0.01) or aortic atherosclerosis (r=-0.524, P<0.01) in SD rats. Experiment 2: sinoaortic denervation (SAD) was performed in SD rats. Then atherosclerosis was also induced. The atherosclerosis scores in SAD rats were significantly higher than those in sham-operated rats (aortic score: 1.50+/-0.41 versus 1.10+/-0.39, P<0.05; coronary score: 1.70+/-0.35 versus 1.25+/-0.54, P<0.05). Using immunohistochemistry and Western blotting methods, it was found that the expressions of C-reactive protein, intercellular adhesion molecule-1 and vascular-cell adhesion molecule-1 in coronary artery and aorta were increased in SAD rats compared with sham-operated rats. These results indicate that arterial baroreflex dysfunction promotes the development of atherosclerosis in rats, and that inflammation may be involved in this process.
authors.affiliation: Department of Pharmacology, Second Military Medical University, 325 Guo He Road, Shanghai 200433, China.
authors.forename: Guo-Jun
authors.initials: GJ
authors.lastname: Cai
authors.forename: Chao-Yu
authors.initials: CY
authors.lastname: Miao
authors.forename: He-Hui
authors.initials: HH
authors.lastname: Xie
authors.forename: Li-Hua
authors.initials: LH
authors.lastname: Lu
authors.forename: Ding-Feng
authors.initials: DF
authors.lastname: Su
mesh_terms: D000818:Animals; D001011:Aorta / Q000737:chemistry / Q000294:innervation / Q000473:pathology / Q000503:physiopathology*; D001018:Aortic Diseases / Q000209:etiology / Q000503:physiopathology; D050197:Atherosclerosis / Q000209:etiology* / Q000503:physiopathology; D017763:Autonomic Denervation; D017704:Baroreflex; D002097:C-Reactive Protein / Q000032:analysis; D002339:Carotid Arteries / Q000294:innervation / Q000503:physiopathology*; D002762:Cholecalciferol / Q000633:toxicity; D004036:Diet, Atherogenic; D006937:Hypercholesterolemia / Q000150:complications; D006973:Hypertension / Q000139:chemically induced / Q000150:complications; D018799:Intercellular Adhesion Molecule-1 / Q000032:analysis; D008297:Male; D009206:Myocardium / Q000737:chemistry / Q000473:pathology; D010656:Phenylephrine / Q000633:toxicity; D051381:Rats; D017207:Rats, Sprague-Dawley; D012021:Reflex, Abnormal / Q000502:physiology*; D019010:Vascular Cell Adhesion Molecule-1 / Q000032:analysis
chemical_list: D019010:Vascular Cell Adhesion Molecule-1; D018799:Intercellular Adhesion Molecule-1; D002762:Cholecalciferol; D010656:Phenylephrine; D002097:C-Reactive Protein