Localization of the ANG II type 2 receptor in the microcirculation of skeletal muscle.
Localization of the ANG II type 2 receptor in the microcirculation of skeletal muscle.
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DOI：
10.1152/ajpheart.1998.275.4.h1395
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发表时间：
1998-10
期刊：
影响因子：
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通讯作者：
E. Nora;D. Munzenmaier;F. Hansen-Smith;J. Lombard;A. Greene
中科院分区：
文献类型：
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作者：
E. Nora;D. Munzenmaier;F. Hansen-Smith;J. Lombard;A. Greene
只有功能研究表明血管紧张素Ⅱ2型(AT2)受体存在于微循环中。为了确定该受体在大鼠骨骼肌微循环中的分布，制备了多克隆兔抗大鼠抗血清，并进行了免疫组织化学和Western印迹分析。制备的抗血清针对AT2受体合成肽，并通过竞争试验和敏感性试验进行了验证。蛋白质印迹分析显示，提睾肌和比目鱼肌在∼40 kDa处有一条明显的单一条带。免疫组织化学分析显示AT2受体广泛分布于骨骼肌大小微血管的微循环中。显微解剖研究显示血管内皮细胞AT2受体的定位，而血管平滑肌α-肌动蛋白双重标记也显示AT2受体与血管平滑肌细胞共定位。其他与微血管相关的细胞也对AT2受体呈阳性染色。简而言之，这项研究证实了先前的功能数据，并将AT2受体定位于微循环。这些研究表明，AT2受体存在于各种类型的血管细胞上，并且其定位方式使其能够直接对抗Ang II 1型受体的作用。
Only functional studies have suggested the presence of the ANG II type 2 (AT2) receptor in the microcirculation. To determine the distribution of this receptor in the rat skeletal muscle microcirculation, a polyclonal rabbit anti-rat antiserum was developed and used for immunohistochemistry and Western blot analysis. The antiserum was prepared against a highly specific and antigenic AT2-receptor synthetic peptide and was validated by competition and sensitivity assays. Western blot analysis demonstrated a prominent, single band at ∼40 kDa in cremaster and soleus muscle. Immunohistochemical analysis revealed a wide distribution of AT2 receptors throughout the skeletal muscle microcirculation in large and small microvessels. Microanatomic studies displayed an endothelial localization of the AT2 receptor, whereas dual labeling with smooth muscle α-actin also showed colocalization of the AT2 receptor with vascular smooth muscle cells. Other cells associated with the microvessels also stained positive for AT2 receptors. Briefly, this study confirms previous functional data and localizes the AT2 receptor to the microcirculation. These studies demonstrate that the AT2 receptor is present on a variety of vascular cell types and that it is situated in a fashion that would allow it to directly oppose ANG II type 1 receptor actions.