Electrophysiological properties of rostral ventrolateral medulla neurons in angiotensin II 1a receptor knockout mice
Electrophysiological properties of rostral ventrolateral medulla neurons in angiotensin II 1a receptor knockout mice
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DOI：
10.1161/01.hyp.0000173421.97463.ac
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发表时间：
2005-08-01
期刊：
影响因子：
8.3
通讯作者：
Saruta, T
中科院分区：
文献类型：
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作者：
Matsuura, T;Kumagai, H;Saruta, T
我们比较了新生血管紧张素II 1a型受体敲除小鼠和野生型小鼠延髓头端腹外侧神经元对血管紧张素II、其1型受体阻断剂坎地沙坦和其2型受体阻断剂PD 123319的电生理特性。利用全细胞膜片钳技术，我们研究了脑干-脊髓标本中的延髓头端腹外侧神经元的特性，其中交感神经元网络被保存。血管紧张素II 1a型受体敲除小鼠和野生型小鼠之间的基线膜电位和放电率几乎相似。灌流血管紧张素II去极化头端腹外侧延髓延髓神经元在野生型小鼠，而它超极化血管紧张素II型1a受体敲除小鼠。由于坎地沙坦预处理显著阻止了野生型小鼠血管紧张素II诱导的去极化，因此血管紧张素II 1型受体对这种去极化至关重要。血管紧张素II 1a型受体敲除小鼠中PD 123319去极化延髓头端腹外侧球脊髓神经元的灌流。PD 123319阻止血管紧张素II 1a型受体敲除小鼠中血管紧张素II诱导的超极化，相反，它诱导去极化。这些结果表明，血管紧张素Ⅱ 2型受体在头端腹外侧延髓发挥拮抗作用，对血管紧张素Ⅱ 1a型受体在控制头端腹外侧延髓的神经元活动。
We compared the electrophysiological properties of neurons in the rostral ventrolateral medulla of neonatal angiotensin II type 1a receptor knockout mice and wild-type mice with responses to angiotensin II, its type-1 receptor blocker candesartan, and its type-2 receptor blocker PD123319. Using the whole-cell patch-clamp technique, we examined the characteristics of rostral ventrolateral medulla neurons in brain stem-spinal cord preparations in which the sympathetic neuronal network is preserved. Baseline membrane potential and firing rate were almost similar between angiotensin II type 1a receptor knockout mice and wild-type mice. Superfusion with angiotensin II depolarized rostral ventrolateral medulla bulbospinal neurons in wild-type mice, whereas it hyperpolarized those in angiotensin II type 1a receptor knockout mice. Because pretreatment with candesartan significantly prevented the angiotensin II-induced depolarization in wild-type mice, the angiotensin II type 1 receptor is crucial for this depolarization. Superfusion with PD123319 depolarized rostral ventrolateral medulla bulbospinal neurons in angiotensin II type 1a receptor knockout mice. PD123319 prevented the angiotensin II-induced hyperpolarization in angiotensin II type 1a receptor knockout mice, and, rather, it induced depolarization. These results suggest that the angiotensin II type 2 receptor in rostral ventrolateral medulla plays an antagonistic role against the angiotensin II type 1a receptor in controlling the neuronal activity of rostral ventrolateral medulla.