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COMMENT ON “PROTECTIVE ARMS OF THERENIN–ANGIOTENSIN SYSTEM INNEUROLOGICAL DISEASE”: REPLY

机译:关于“神经疾病中肾素-血管紧张素系统的保护臂”的评论:答复

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We thank Drs Smith and Muralidharan for their interest in ourreview article,1which was updating recent neurological researchrelated to the angiotensin (Ang) II AT2receptor (AT2R), includ-ing their own recent data. The following reply addresses theircomments.First, as stated twice on p. 582 of our article, we believe thatPD123319 is a standard tool in AT2R research and we neverquestioned that it has AT2R antagonistic properties.1Second, thecorrect citation of our article is as follows:Two very recent publications provide experimental evidencethat EMA401 and analogues indeed reduce neurite density ofhuman dorsal root ganglia and neurite length in AngII-treated ratdorsal root ganglia and that they exert antinociceptive actions.2,3However, neither of these two studies provided conclusive proofthat the compounds tested are AT2R antagonists.
机译:感谢Smith和Muralidharan博士对我们的综述文章1的关注,该文章正在更新与血管紧张素II(AT)2受体(AT2R)有关的最新神经系统研究,包括其自身的最新数据。以下答复解决了他们的意见:首先,如第2页所述。在本文的582中,我们认为PD123319是AT2R研究的标准工具,我们毫不怀疑它具有AT2R拮抗特性。1其次,本文的正确引述如下:两个非常新的出版物提供了实验证据,表明EMA401和类似物确实降低了神经突密度。 AngII处理的大鼠背根神经节中的人背根神经节和神经突长度,它们均具有镇痛作用。2,3然而,这两项研究均未提供确凿的证据证明所测试的化合物是AT2R拮抗剂。

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