Li-Li Zhang1,2, Ying Zhang1, Yan-Qiong Cheng1,3, Jing-Ming Zhang1, Hong-Qi Liu1, Wei-Zhong Wang4, Jawahar L Mehta5, Zhi-Gang Xiong6, Ding-Feng Su1, Ai-Jun Liu1. 1. Department of Pharmacology, School of Pharmacy, Second Military Medical University, Shanghai, China. 2. Department of Pharmacy, Fuzhou General Hospital of Nanjing Military Command PLA, Fuzhou, China. 3. Department of Urology, Changhai Hospital, Second Military Medical University, Shanghai, China. 4. Department of Physiology, Second Military Medical University, Shanghai, China. 5. Internal Medicine, Physiology and Biophysics, Stebbins Chair in Cardiology, Division of Cardiovascular Medicine, University of Arkansas for Medical Sciences, Little Rock, AR, USA. 6. Department of Neurobiology, Morehouse School of Medicine, Atlanta, GA, USA.
Abstract
AIMS: It is unclear whether the impaired BRS plays a key role in the incidence of cardiovascular diseases. The molecular mechanism of impaired BRS remains to be fully elucidated. We hypothesized that selection of rats based on deficient and normal intrinsic BRS would yield models that reflect cardiovascular diseases risk. METHODS AND RESULTS: Twenty generations of selection produced arterial baroreflex low rats and normal rats that differed in BRS by about 2.5-fold change. Metabolic syndrome (including hypertension, overweight, hyperlipemia, and hyperglycemia) emerged in ABR-DRs. Although ABR-DRs consumed less food, they gained significantly more body weight. CONCLUSION: Our study demonstrated that intrinsic low BRS induced hypertension and metabolic disorder. Restoration of impaired BRS might be a potent target of therapeutic intervention in metabolic syndrome.
AIMS: It is unclear whether the impaired BRS plays a key role in the incidence of cardiovascular diseases. The molecular mechanism of impaired BRS remains to be fully elucidated. We hypothesized that selection of rats based on deficient and normal intrinsic BRS would yield models that reflect cardiovascular diseases risk. METHODS AND RESULTS: Twenty generations of selection produced arterial baroreflex low rats and normal rats that differed in BRS by about 2.5-fold change. Metabolic syndrome (including hypertension, overweight, hyperlipemia, and hyperglycemia) emerged in ABR-DRs. Although ABR-DRs consumed less food, they gained significantly more body weight. CONCLUSION: Our study demonstrated that intrinsic low BRS induced hypertension and metabolic disorder. Restoration of impaired BRS might be a potent target of therapeutic intervention in metabolic syndrome.
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