Nobiling R, Bührle C P, Hackenthal E, Helmchen U, Steinhausen M, Whalley A, Taugner R
Virchows Arch A Pathol Anat Histopathol. 1986;410(1):31-42. doi: 10.1007/BF00710903.
Histological, ultrastructural, immunohistochemical, intravital microscopic and electrophysiological techniques have been applied to study experimental hydronephrosis in rats in order to assess its value as a preparation for the investigation of renal microcirculation and of the electrophysiological properties of the renin-containing juxtaglomerular (JG) cells of the afferent glomerular arteriole. As hydronephrosis develops, the kidney parenchyma becomes progressively thinner owing to tubular atrophy. Twelve weeks after ureteral ligature, this process results in a transparent tissue sheet of about 150-200 microns in thickness. In this preparation, the renal arterial tree as well as the glomeruli can be easily visualized for intravital microscopic studies, e.g. the determination of kidney vessel diameters, or the identification of JG cells for penetration with an intracellular microelectrode. In contrast to the tubular atrophy, the vascular system is well preserved, and the JG cells and the sympathetic axon terminals are ultrastructurally intact. This is also true for the glomeruli, except for a certain confluence of the podocyte foot processes and a thickening of the basal laminae. Renin immunostaining and kidney renin content in the hydronephrotic organ correspond to those in control kidneys. In addition, there are no differences in the plasma renin levels of hydronephrotic and control rats. Intravital microscopic observations reveal that the renal vascular tree reacts in a typical, concentration dependent manner to the vasoconstrictor agent angiotensin II, mainly at the level of the resistance vessels. Electrophysiological recordings from juxtaglomerular granulated cells show a high membrane potential (-60 mV), and spontaneous depolarizing junction potentials, owing to random transmitter release from the nerve terminals. Angiotensin II, an inhibitor of renin release, depolarizes JG cells reversibly. Hence, we may infer that the hydronephrotic rat kidney is a suitable model for in vivo studies of the renal microcirculation as well as for in vitro investigations of the electrophysiological properties of the media cells of the afferent glomerular arteriole.
组织学、超微结构、免疫组织化学、活体显微镜检查和电生理技术已被应用于研究大鼠实验性肾积水，以评估其作为研究肾微循环以及入球小动脉含肾素的球旁（JG）细胞电生理特性的一种制备模型的价值。随着肾积水的发展，由于肾小管萎缩，肾实质逐渐变薄。输尿管结扎12周后，这一过程导致形成一层厚度约为150 - 200微米的透明组织薄片。在此制备模型中，肾动脉树以及肾小球在活体显微镜研究中很容易被观察到，例如用于测定肾血管直径，或识别JG细胞以便用细胞内微电极进行穿刺。与肾小管萎缩不同，血管系统保存完好，JG细胞和交感神经轴突终末在超微结构上是完整的。肾小球也是如此，只是足细胞足突有一定融合且基膜增厚。肾积水器官中的肾素免疫染色和肾素含量与对照肾脏中的相当。此外，肾积水大鼠和对照大鼠的血浆肾素水平没有差异。活体显微镜观察显示，肾血管树对血管收缩剂血管紧张素II以典型的浓度依赖性方式作出反应，主要在阻力血管水平。对球旁颗粒细胞的电生理记录显示其具有较高的膜电位（-60 mV），并且由于神经末梢随机释放递质而出现自发去极化的连接电位。血管紧张素II是肾素释放的抑制剂，可使JG细胞可逆性去极化。因此，我们可以推断，肾积水大鼠肾脏是用于肾微循环体内研究以及入球小动脉中膜细胞电生理特性体外研究的合适模型。
