Work

High salt induced hypertension leads to cognitive defect

Year: 2017

Type: article

Abstract: // Cui-Ping Guo 1 , Zhen Wei 1 , Fang Huang 1 , Min Qin 1 , Xing Li 1 , Yu-Man Wang 1 , Qun Wang 1 , Jian-Zhi Wang 1, 2 , Rong Liu 1 , Bin Zhang 3 , Hong-Lian Li 4 and Xiao-Chuan Wang 1, 2 1 Department 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 2 Division of Neurodegenerative Disorders, Co-innovation Center of Neuroregeneration, Nantong University, Nantong, JS 226001, China 3 Department of Genetics and Genomic Sciences, Icahn School of Medicine at Mount Sinai, New York, NY 10029, USA 4 Department 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 Correspondence to: Xiao-Chuan Wang, email: [email protected] Hong-Lian Li, email: [email protected] 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 ABSTRACT 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.

Source: Oncotarget

DOI: 10.18632/oncotarget.21326