ANGIOTENSIN-II TYPE-2 RECEPTOR-MODULATED CHANGES IN POTASSIUM CURRENTS IN CULTURED NEURONS
ANGIOTENSIN-II TYPE-2 RECEPTOR-MODULATED CHANGES IN POTASSIUM CURRENTS IN CULTURED NEURONS
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DOI：
10.1152/ajpcell.1993.265.3.c607
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发表时间：
1993-09-01
影响因子：
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通讯作者：
POSNER, P
中科院分区：
文献类型：
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作者：
KANG, J;SUMNERS, C;POSNER, P
我们先前已经证明，血管紧张素II(Ang II)刺激共培养的新生大鼠下丘脑和脑干神经元的净外向离子电流(I(NO))增加，这种作用是由Ang II 2型(AT2)受体介导的。I(NO)主要由K+和Ca~(2+)电流组成，在本研究中，我们使用全细胞电压钳程序来确定其中哪些电流是由AT2受体调制的。我们发现Ang II(50-100 nM)对培养神经元既有瞬时钾电流(I(A))，又有延迟整流钾电流(I(K))。这种作用是由AT2受体介导的(可被1MU的PD-123177阻断，但不被1MU的氯沙坦阻断)。对于I(A)和I(K)，Ang II均引起最大电导增加。相反，Ang II既不改变钙激活的钾电流，也不改变钙电流。我们的数据证实了血管紧张素Ⅱ对培养的新生神经细胞I(A)和I(K)的离散AT2受体介导的作用。重要的是，这些数据为大脑中这种Ang II受体亚型介导的行为或生理效应(尚未确定)提供了电生理学基础。
We have previously shown that angiotensin II (ANG II) stimulates an increase in net outward ionic current (I(no)) in neurons cocultured from neonate rat hypothalamus and brain stem, an effect mediated by ANG II type 2 (AT2) receptors. I(no) consists mainly of K+ and Ca2+ currents, and in the present study we used whole cell voltage clamp procedures to define which of these currents are modulated by AT2 receptors. We determined that ANG II (50-100 nM) stimulated both transient K+ current (I(A)) and delayed-rectifier K+ current (I(K)) in cultured neurons. The effects were mediated by AT2 receptors (blocked by 1 muM PD-123177 but not by 1 muM losartan). For both I(A) and I(K), ANG II elicited an increase in maximal conductance. By contrast, ANG II altered neither Ca2+-activated K+ current nor Ca2+ current. Our data demonstrate discrete AT2 receptor-mediated effects of ANG II on I(A) and I(K) in cultured neonate neurons. Importantly, these data provide an electrophysiological basis for behavioral or physiological effects (as yet undefined) mediated by this ANG II receptor subtype in the brain.