RENAL MICROVASCULATURE IN HYPERTENSION

肾脏在血压调节中起着重要作用。有一个 肾血管参数(肾血流量和肾脏)的改变 血管阻力)在高血压病和高血压的早期 自发性高血压大鼠(SHR)，一种遗传性高血压大鼠模型。 肾血管改变会影响肾功能，因为血管和 肾小管功能通过自动调节错综复杂地联系在一起 机械装置。因此，肾血管的改变可能参与了 血压升高的发生和维持。这个 拟议的项目将检查肾传入小动脉(主要 肾脏阻力血管)建立遗传性高血压大鼠模型 (冈本SHR)从出生到18周来确定 肾微血管在高血压发病中的作用。传入 小动脉直径将在肾血管铸型中确定，研究人员 SHR、WKY(Wistar京都)和Wistar大鼠的扫描电子显微镜。 直径测量将在有和没有最大直径的动物身上进行。 血管扩张。血管扩张将允许评估相对的 外源性(血管收缩)和内源性(血管)的作用 结构)因素在高血压肾血管病变中的差异。 肾传入小动脉的平滑肌细胞将被检查 扫描和透射电子显微镜。形态测量学方法将 用来分析光滑细胞的整体细胞大小和细胞学特征 高血压大鼠和正常血压大鼠品系的肌细胞 新生儿至18周。与以下各项相关的结构性差异和/或变化 高血压的发展和维持将被确定。这 项目将提供关于肾脏和肾脏之间关系的信息 微血管系统与高血压的发生和发展 血管平滑肌细胞分化的综合检测 血压正常和高血压的动物。这些数据将提供洞察力 从血管方面探讨高血压的发病机制及相关 血管发生了变化。该项目的长期目标是：(1) 肾微血管构筑与血压的关系 调节与高血压，(2)了解血管的个体发生 血管内皮细胞及其改变可能与血管病变的发病机制有关 高血压和(3)了解是什么调节了平滑肌细胞 肾的分化，包括正常和异常。

The kidneys play a major role in blood pressure regulation. There is an alteration of renal vascular parameters (renal blood flow and renal vascular resistance) early in essential hypertension as well as in the spontaneously hypertensive rat (SHR), a genetic rat model of hypertension. Renal vascular alterations can affect renal function because vascular and tubular functions are intricately linked through auto-regulatory mechanisms. Therefore, the renal vascular alterations may contribute to the development and maintenance of the elevated blood pressure. The proposed project will examine the renal afferent arteriole (the major resistance vessel in the kidney) in a genetic rat model of hypertension (the Okamoto SHR) from birth through 18 weeks to ascertain the role of the renal microvasculature in the development of hypertension. Afferent arteriolar diameters will be determined in renal vascular casts, studied by scanning electron microscopy in SHR, WKY (Wistar Kyoto) and Wistar rats. Diameter measurements will be made in animals with and without maximal vasodilation. The vasodilation will allow an assessment of relative contributions of extrinsic (vasoconstriction) and intrinsic (vascular structure) factors in the renal vascular differences in hypertension. Smooth muscle cells of renal afferent arterioles will be examined by scanning and transmission electron microscopy. Morphometric methods will be used to analyze whole cell size and cytologic features of the smooth muscle cells in hypertensive and normotensive rat strains at ages from newborn to 18 weeks. Structural differences and/or changes associated with the development and maintenance of hypertension will be identified. This project will provide information on the relationship between the renal microvasculature and the development of hypertension as well as a comprehensive examination of vascular smooth muscle cell differentiation in normotensive and hypertensive animals. These data will provide insight into vascular aspects of the pathogenesis of hypertension and associated vascular changes. The long term objectives of the project are (1) to determine the relationship of the renal microvasculature to blood pressure regulation and hypertension, (2) to understand the ontogenesis of vascular smooth muscle cells and alteration which may relate to the pathogenesis of hypertension and (3) to understand what regulates smooth muscle cell differentiation in the kidney, both normal and abnormal.