Gelband C H, Zhu M, Lu D, Reagan L P, Fluharty S J, Posner P, Raizada M K, Sumners C
Department of Physiology, University of Florida, College of Medicine, Gainesville 32610, USA.
Endocrinology. 1997 May;138(5):2195-8. doi: 10.1210/endo.138.5.5236.
Angiotensin II (Ang II), via the activation of the AT1 and AT2 receptors regulates electrophysiological responses of catecholaminergic neurons. This study was designed to determine if functional interactions between AT1 and AT2 receptors exist in a single neuron. Ang II caused two unique electrophysiological responses characteristic of receptor crosstalk. First, Ang II elicited an AT1 receptor-mediated decrease in I(K) followed by an AT2 receptor-mediated increase in I(K). Second, Ang II elicited an AT2 receptor-mediated increase in I(K) followed by an AT1 receptor-mediated decrease in I(K). AT1 and AT2 receptors were co-localized on the catecholaminergic neurons. These observations suggest, for the first time, the existence of a crosstalk between Ang II receptor subtypes that may be significant in the physiological activity of catecholaminergic neurons.
血管紧张素II（Ang II）通过激活AT1和AT2受体来调节儿茶酚胺能神经元的电生理反应。本研究旨在确定AT1和AT2受体之间的功能相互作用是否存在于单个神经元中。Ang II引发了两种受体串扰特有的独特电生理反应。首先，Ang II引发了由AT1受体介导的I(K)降低，随后是由AT2受体介导的I(K)增加。其次，Ang II引发了由AT2受体介导的I(K)增加，随后是由AT1受体介导的I(K)降低。AT1和AT2受体共定位于儿茶酚胺能神经元上。这些观察结果首次表明，血管紧张素II受体亚型之间存在串扰，这可能在儿茶酚胺能神经元的生理活动中具有重要意义。
