Protective effects of angiotensin receptor control on ischemic neuronal injury

已知脑缺血后线粒体凋亡介导神经元损伤。血管紧张素II型1受体激活导致超氧化物的产生，但血管紧张素II型1受体阻断是否阻止缺血后线粒体凋亡尚不清楚。正常血压大鼠在全脑缺血诱导前给予血管紧张素II型1受体阻滞剂、坎地沙坦或单药。在坎地沙坦处理的动物中，大约30%的海马CA1神经元存活，而在载药处理的动物中，只有2%的神经元存活。坎地沙坦处理动物的这些脆弱神经元中超氧化物的产生和细胞色素c的释放明显少于载药处理动物。血管紧张素II型1受体可能在全脑缺血后易损神经元凋亡细胞死亡中起重要作用。

Mitochondrial apoptosis after cerebral ischemia is known to mediate neuronal injury. Angiotensin II type 1 receptor activation results in production of superoxide, but whether angiotensin II type 1 receptor blockade prevents mitochondrial apoptosis after ischemia remains unclear. Normotensive rats received the angiotensin II type 1 receptor blocker, candesartan or only vehicle before induction of global cerebral ischemia. Approximately 30% of the hippocampal CA1 neurons survived in candesartan-treated animals, whereas only 2% of neurons survived in vehicle-treated animals. Superoxide production and cytochrome c release were significantly less in these vulnerable neurons in candesartan-treated animals than in vehicle-treated animals. Angiotensin II type 1 receptor may have an essential role in apoptotic cell death in vulnerable neurons after global cerebral ischemia.