Amelioration of ischemic neuronal by angiotensin receptor control

脑缺血后过多的超氧化物产生被认为是介导神经元损伤的因素。血管紧张素II 1型受体的激活导致超氧化物的产生，但血管紧张素II 1型受体阻断是否能阻止超氧化物的产生和随后的缺血后神经元损伤仍不清楚。血压正常的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单独使用。在坎地沙坦治疗的动物中，大约30%的海马CA1神经元存活，而在赋形剂治疗的动物中，只有2%的神经元存活。在坎地沙坦治疗的动物中，这些脆弱的神经元中超氧化物的产生明显少于赋形剂治疗的动物。血管紧张素II 1型受体可能在全脑缺血后易损神经元产生超氧化物和随后的损伤中起重要作用。

Excessive superoxide production 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 production of superoxide and subsequent neuronal injury 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 was 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 superoxide production and subsequent injury in vulnerable neurons after global cerebral ischemia.