Siffert W
Institut für Pharmakologie, Universitätsklinikum Essen, Germany.
Kidney Blood Press Res. 1996;19(3-4):172-3. doi: 10.1159/000174067.
Recent studies have shown that enhanced Na/H exchanger activity, a frequently observed abnormality in essential hypertension, persists in Epstein-Barr-virus-immortalised lymphoblasts from afflicted patients. This phenomenon is associated with an enhanced proliferation of these cell lines. Studies have ruled out structural changes in the Na/H exchanger protein, but demonstrated a distinct enhancement of intracellular signal transduction in these cell lines. The ultimate cause can be assigned to an obviously genetically fixed increased reactivity of pertussis-toxin-sensitive G proteins, which can easily explain the increased formation of intracellular- second messengers, enhanced Ca2+ signals, and enhanced proliferation of these cell lines. Thus, hypertension in the subset of patients with enhanced Na/H exchanger activity could be caused by increased G protein reactivity.
最近的研究表明，钠/氢交换体活性增强是原发性高血压中常见的异常现象，在患病患者的爱泼斯坦-巴尔病毒永生化淋巴细胞中持续存在。这种现象与这些细胞系的增殖增强有关。研究排除了钠/氢交换体蛋白的结构变化，但证明了这些细胞系中细胞内信号转导明显增强。最终原因可归因于百日咳毒素敏感的G蛋白反应性明显的基因固定增加，这很容易解释细胞内第二信使形成增加、钙信号增强以及这些细胞系的增殖增强。因此，钠/氢交换体活性增强的患者亚组中的高血压可能是由G蛋白反应性增加引起的。
