Edvinsson Lars
Department of Medicine, University Hospital, Lund University, 22185 Lund, Sweden.
Trends Cardiovasc Med. 2008 Apr;18(3):98-103. doi: 10.1016/j.tcm.2008.01.005.
The mechanism behind the positive response to the inhibition of the angiotensin II receptor AT(1) in conjunction with stroke is elusive. Here we demonstrate that cerebrovascular AT(1) receptors show increased expression (upregulation) after cerebral ischemia via enhanced translation. This enhanced expression of AT(1) receptors occurs in the ischemic cerebral arteries and microvessels, and their inhibition results in a reduction in infarct volume. These findings add to the understanding of the vascular component in stroke, and the identified inhibition provides a new way to reduce the extent of cerebral ischemic damage.
血管紧张素 II 受体 AT(1) 抑制与中风相关的阳性反应背后的机制尚不清楚。在此，我们证明脑血管 AT(1) 受体在脑缺血后通过增强翻译表现出表达增加（上调）。AT(1) 受体的这种增强表达发生在缺血性脑动脉和微血管中，对其抑制会导致梗死体积减小。这些发现增进了对中风中血管成分的理解，并且所确定的抑制作用为减少脑缺血损伤程度提供了一种新方法。
