High salt induced hypertension leads to cognitive defect
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Cui-Ping Guo1, Zhen Wei1, Fang Huang1, Min Qin1, Xing Li1, Yu-Man Wang1, Qun Wang1, Jian-Zhi Wang1,2, Rong Liu1, Bin Zhang3, Hong-Lian Li4 and Xiao-Chuan Wang1,2
1Department of Pathophysiology, School of Basic Medicine, Key Laboratory of Ministry of Education of China for Neurological Disorders, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, China
2Division of Neurodegenerative Disorders, Co-innovation Center of Neuroregeneration, Nantong University, Nantong, JS 226001, China
3Department of Genetics and Genomic Sciences, Icahn School of Medicine at Mount Sinai, New York, NY 10029, USA
4Department of Histology and Embryology, School of Basic Medicine, Key Laboratory of Ministry of Education of China for Neurological Disorders, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, China
Xiao-Chuan Wang, email: firstname.lastname@example.org
Hong-Lian Li, email: email@example.com
Keywords: high salt diet; hypertension; cognitive defects; synaptogenesis; cerebral blood flow
Abbreviations: AD: Alzheimer’s disease; BP: blood pressure; SBP: systolic blood pressure; CBF: cerebral blood flow
Received: July 27, 2017 Accepted: August 17, 2017 Published: September 27, 2017
Although increasing evidences suggest a relationship between hypertension and brain function for years, it is still unclear whether hypertension constitutes a risk factor for cognitive decline and its underlying mechanism. In the present study, an experimental animal model of hypertension simply by feeding rats with high salt diet was employed. We found that long-term high salt intake caused a marked increase of systolic blood pressure linked to a declined regional cerebral blood flow. Fear conditioning and morris water maze behavioral test revealed that high salt diet induced hippocampal dependent spatial reference memory deficits, while a decreased synaptogenesis without neuronal loss in hippocampus was observed in high salt treated rats. Furthermore, we found that high salt induced a decrease of intracellular calcium, which inactivated CaMK II and resulted in dephosphorylation of CREB at Ser133. These findings suggest a novel etiopathogenic mechanism of cognitive deficit induced by hypertension, which is initiated by high salt diet.
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