Renal bradykinin receptors: localisation, transduction pathways and molecular basis for a possible pathological role (review).
Renal bradykinin receptors: localisation, transduction pathways and molecular basis for a possible pathological role (review).
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肾缓激肽受体：定位、转导途径和可能病理作用的分子基础（综述）。
DOI：
10.3892/ijmm.3.2.185
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发表时间：
1999
影响因子：
5.4
通讯作者：
J. Bascands
中科院分区：
文献类型：
--
作者：
J. Schanstra;C. Alric;M. Marin;J. Girolami;J. Bascands
激肽是一种具有生物活性的多肽，它通过激活两个七跨膜G蛋白偶联受体B1和B2发挥作用，这两个受体的同源性仅为36%。生理条件下的主要激肽肽，缓激肽（BK），调节肾血流动力学和功能。在生理条件下，大多数BK效应涉及缓激肽B2受体。对细胞内转导途径的研究、这些受体沿肾单位沿着的表达和定位的调节，以及对转基因小鼠模型的首次研究，已经允许更好地定义这些受体在生理和病理条件下的作用。肾脏B1受体的作用，在各种炎症相关的病理诱导，知之甚少。最近对B1受体诱导的分子机制及其详细的肾脏定位的研究表明，在炎症条件下，这种激肽受体可能是重要的。B2受体被认为参与了血管紧张素转换酶（ACE）抑制剂在胰岛素依赖型糖尿病中的肾保护作用。然而，ACE抑制剂治疗也导致B1激动剂浓度增加，可能导致B1受体的同源诱导和激活。
Kinins are biologically active peptides that exert their effects by activating two seven transmembrane G-protein coupled receptors termed B1 and B2 which have only about 36% of homology. The major kinin peptide under physiological conditions, bradykinin (BK), modulates renal haemodynamics and function. Under physiological conditions most BK effects involve bradykinin B2-receptors. Studies on the intra-cellular transduction pathways, the regulation of the expression and the localisation of these receptors along the nephron, as well as the first studies on transgenic mice models, have allowed to better define the role of these receptors under physiological and pathological conditions. The role of the renal B1-receptor, induced in a variety of pathologies related to inflammation, is poorly understood. Recent investigations on the molecular mechanism of B1-receptor induction and its detailed renal localisation have shown that under inflammatory conditions this kinin receptor might be of importance. B2-receptors are suggested to be involved in part of the renoprotective effects of angiotensin converting enzyme (ACE)-inhibitors in insulin-dependent diabetes. However, ACE-inhibitor treatment, resulting also in an increased B1-agonist concentration might result in homologous induction and activation of the B1-receptor.