皮质N-甲基-D-酸盐 (NMDA) 受体通过影响脏自我调节来调解脏血管扩张
Cesar A Romero1, Jasmine Lim1, Hong Wang2
1Renal Division, Department of Medicine, Emory University School of Medicine, Atlanta, Georgia, USA.
bioRxiv : the preprint server for biology
|December 18, 2023
概括
上皮细胞中的N-甲基-D-酸盐受体 (NMDAR) 促进 afferent动脉血管扩张. 这一过程涉及通过管状球体反激活ENaC通道,特别是在雌性小鼠中.
科学领域:
- 腎臟病學 (nephrology) 是一種醫學專業.
- 分子生物学分子生物学
- 生理学 生理学 生理学
背景情况:
- N-甲基-D-酸盐受体 (NMDARs) 对于大脑功能至关重要,但它们在生理学中的作用在很大程度上是未知的.
- NMDAR 抑制剂会影响血清和淋巴细胞过率 (GFR),这表明功能.
- 我们研究了NMDARs在远端脏在通过连接管管-球膜反 (CNTGF) 和ENaC激活来调节 afferent arteriole血管扩张中的作用.
研究的目的:
- 为了研究NMDARs在脏中的表达和功能.
- 确定远端脏中的NMDAR是否通过CNTGF调节脏血液流动.
- 阐明NMDARs和ENaC在调解血管扩张中的相互作用.
主要方法:
- 对管体特异性转录组数据库的分析.
- 分子生物学和显微镜技术检测细胞中的NMDAR亚单元表达.
- 在小鼠脏中进行NMDAR激动剂和阻断剂的体外微 perfusion.
- 在体内进行脏微穿孔,以测量停止流量压力.
- 使用mpkCCD细胞和分裂开放管道的电生理学研究来评估ENaC活动.
主要成果:
- NMDAR子单元表达在脏沿线,特别是ENaC阳性细胞中,在雌性小鼠中表达的数量更高.
- 连接管中的NMDAR激活诱导了依赖CNTGF和ENaC活动的 afferent-arteriole血管扩张.
- 在体内研究证实,在NMDAR激活后,CNTGF相关的血管扩张.
- 激活NMDAR会增加氨酸敏感电流和细胞中的ENaC活性.
结论:
- 表皮NMDARs存在于脏中,包括表达ENaC的细胞,表达的性别差异.
- 皮质NMDAR通过CNTGF通过增强ENaC活性来调解血管扩张.
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