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Arterial baroreflex dysfunction promotes atherosclerosis in rats.

Guo-Jun Cai·Chao-Yu Miao·He-Hui Xie·Li-Hua Lu·Ding-Feng Su
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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.

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AnimalsAortaAortic DiseasesAtherosclerosisAutonomic DenervationBaroreflexC-Reactive ProteinCarotid ArteriesCholecalciferolDiet, AtherogenicHypercholesterolemiaHypertensionIntercellular Adhesion Molecule-1MaleMyocardiumPhenylephrineRatsRats, Sprague-DawleyReflex, AbnormalVascular Cell Adhesion Molecule-1Journal ArticleResearch Support, Non-U.S. Gov't

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Guo-Jun Cai, Chao-Yu Miao, He-Hui Xie, Li-Hua Lu, Ding-Feng Su. 2005. Arterial baroreflex dysfunction promotes atherosclerosis in rats.. https://doi.org/10.1016/j.atherosclerosis.2005.03.037

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