High salt induced hypertension leads to cognitive defect.

High salt induced hypertension leads to cognitive defect.
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高盐高血压导致认知缺陷

DOI:
10.18632/oncotarget.21326
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发表时间:
2017-11-10
期刊:
影响因子:
--
通讯作者:
Wang XC
Wang XC
中科院分区:
其他
文献类型:
--
作者:
Guo CP;Wei Z;Huang F;Qin M;Li X;Wang YM;Wang Q;Wang JZ;Liu R;Zhang B;Li HL;Wang XC

文献摘要

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虽然近年来越来越多的证据表明高血压与脑功能的关系,但高血压是否构成认知功能下降的危险因素及其潜在机制仍不清楚。本研究采用高盐饮食喂养大鼠,建立高血压动物模型。我们发现,长期高盐摄入会导致收缩压显著升高,这与局部脑血流量下降有关。恐惧条件反射和morris水迷宫行为学实验表明,高盐饮食可导致大鼠海马依赖性空间参考记忆障碍,同时观察到高盐饮食处理的大鼠海马突触发生减少,但无神经元丢失。此外,我们发现,高盐诱导细胞内钙的减少,这灭活CaMK II,并导致CREB的Ser133去磷酸化。提示高盐饮食是高血压认知功能障碍的一个新的发病机制。
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.