Protective effects of angiotensin receptor control on ischemic neuronal injury

脑缺血后线粒体凋亡介导神经元损伤。血管紧张素II 1型受体激活导致超氧化物的产生，但血管紧张素II 1型受体阻断剂是否能防止缺血后线粒体凋亡仍不清楚。正常血压大鼠在诱导全脑缺血前接受血管紧张素II 1型受体阻滞剂坎地沙坦或仅接受溶媒。坎地沙坦处理的动物中大约30%的海马CA1神经元存活，而溶剂处理的动物中仅2%的神经元存活。在坎地沙坦处理的动物中，这些脆弱的神经元中的超氧化物产生和细胞色素c释放显著低于溶剂处理的动物。血管紧张素Ⅱ 1型受体可能在全脑缺血后脆弱神经元的凋亡中起重要作用。

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.