Electrophysiological responses of angiotensin peptides on the rat isolated nodose ganglion.

R E Widdop, E Krstew, B Jarrott
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引用次数: 28

Abstract

Previous autoradiographic studies have identified angiotensin II (AII) binding sites over the nodose ganglion and along the vagal afferent neurons. In the present study, we examined whether these binding sites are functional receptors by measuring d.c. potential changes by extracellular recording techniques in the rat isolated nodose ganglion preparation in response to superfusion of angiotensin peptides. It was found that AII, as well as AI and AIII elicited concentration-dependent depolarisation of the nodose ganglion. However, the amino terminal angiotensin heptapeptide, A(1-7), failed to evoke any significant response. The AII receptor antagonist, saralasin had no intrinsic activity, but caused a concentration-dependent blockade of AII-induced depolarisation. This study provides evidence for direct neuronal effects of angiotensin peptides on rat vagal afferent neurons. Moreover, this preparation is a relatively convenient one in which to study functional neuronal AII receptor mechanisms on central or peripheral terminals of vagal sensory neurons.

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血管紧张素肽对大鼠离体结节神经节的电生理反应。
先前的放射自显影研究已经确定了血管紧张素II (AII)在结节神经节和迷走神经传入神经元上的结合位点。在本研究中,我们通过细胞外记录技术测量大鼠离体结节神经节制备中血管紧张素肽过剩时的直流电位变化,来检测这些结合位点是否是功能性受体。结果表明,AII以及AII和AIII可引起结节神经节的浓度依赖性去极化。然而,氨基末端血管紧张素七肽A(1-7)没有引起任何显著的反应。AII受体拮抗剂saralasin没有内在活性,但对AII诱导的去极化产生浓度依赖性阻断。本研究为血管紧张素肽对大鼠迷走神经传入神经元的直接作用提供了证据。此外,这种制备方法是研究迷走感觉神经元中枢或外周末梢功能性神经元AII受体机制的一种相对方便的制备方法。
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