Cerebral Autoregulation in Hypertension and Ischemic Stroke: A Mini Review.

Journal of pharmaceutical sciences and experimental pharmacology Pub Date : 2017-01-01 Epub Date: 2017-10-27
Shashank Shekhar, Ruen Liu, Olivia K Travis, Richard J Roman, Fan Fan
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Abstract

Aging and chronic hypertension are associated with dysfunction in vascular smooth muscle, endothelial cells, and neurovascular coupling. These dysfunctions induce impaired myogenic response and cerebral autoregulation, which diminish the protection of cerebral arterioles to the cerebral microcirculation from elevated pressure in hypertension. Chronic hypertension promotes cerebral focal ischemia in response to reductions in blood pressure that are often seen in sedentary elderly patients on antihypertensive therapy. Cerebral autoregulatory dysfunction evokes Blood-Brain Barrier (BBB) leakage, allowing the circulating inflammatory factors to infiltrate the brain to activate glia. The impaired cerebral autoregulation-induced inflammatory and ischemic injury could cause neuronal cell death and synaptic dysfunction which promote cognitive deficits. In this brief review, we summarize the pathogenesis and signaling mechanisms of cerebral autoregulation in hypertension and ischemic stroke-induced cognitive deficits, and discuss our new targets including 20-Hydroxyeicosatetraenoic acid (20-HETE), Gamma-Adducin (Add3) and Matrix Metalloproteinase-9 (MMP-9) that may contribute to the altered cerebral vascular function.

高血压和缺血性脑卒中中的脑自动调节:一个小综述。
衰老和慢性高血压与血管平滑肌、内皮细胞和神经血管耦合功能障碍有关。这些功能障碍会导致肌肉生成反应和大脑自我调节受损,从而降低高血压患者脑小动脉对大脑微循环的保护作用。慢性高血压促进脑局灶性缺血对血压降低的反应,这常见于久坐的老年患者抗高血压治疗。大脑自身调节功能障碍引起血脑屏障(BBB)渗漏,使循环炎症因子渗入大脑激活神经胶质。大脑自调节功能受损引起的炎症和缺血性损伤可导致神经元细胞死亡和突触功能障碍,从而促进认知障碍。在本文中,我们就高血压和缺血性脑卒中引起的认知缺陷的脑自动调节的发病机制和信号机制进行了综述,并讨论了可能导致脑血管功能改变的新靶点,包括20-羟基二碳四烯酸(20-HETE)、γ -内收蛋白(Add3)和基质金属蛋白酶-9 (MMP-9)。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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