RENAL MICROVASCULATURE IN HYPERTENSION

肾脏在血压调节中起主要作用。 有一个 肾血管参数（肾血流量和肾血流）的改变 血管阻力）在原发性高血压早期以及 自发性高血压大鼠（SHR），一种遗传性高血压大鼠模型。 肾血管改变可影响肾功能，因为血管和 肾小管功能通过自动调节 机制等 因此，肾血管改变可能有助于 血压升高的发展和维持。 的 拟议的项目将检查肾传入小动脉（主要 肾脏中的阻力血管）的遗传性高血压大鼠模型中 (the Okamoto SHR）从出生到18周，以确定 肾微血管在高血压发生发展中的作用 传入 将在肾血管铸型中测定小动脉直径， 扫描电子显微镜观察SHR、WKY（Wistar京都）和Wistar大鼠。 将在具有和不具有最大直径的动物中进行直径测量。 血管舒张 血管舒张将允许评估相对 外源性（血管收缩）和内源性（血管收缩）的作用 高血压病肾血管差异的结构因素。 将通过以下方法检查肾传入小动脉的平滑肌细胞： 扫描和透射电子显微镜。 形态测量方法将 用于分析光滑的细胞的全细胞大小和细胞学特征， 高血压和正常血压大鼠品系的肌细胞， 新生儿18周 结构性差异和/或变化 将确定高血压的发展和维持。 这 该项目将提供有关肾功能 微血管和高血压的发展以及 血管平滑肌细胞分化的全面检查， 正常血压和高血压动物。 这些数据将提供洞察力 血管方面的发病机制的高血压和相关的 血管变化 该项目的长期目标是（1） 确定肾微血管与血压的关系 调节与高血压;（2）了解血管的个体发生 平滑肌细胞和改变，可能与发病机制 高血压和（3）了解什么调节平滑肌细胞 肾脏的分化，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.