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小鼠肾积水肾脏作为一种用于含肾素细胞活体显微镜检查和体外电生理研究的工具。

The hydronephrotic kidney of the mouse as a tool for intravital microscopy and in vitro electrophysiological studies of renin-containing cells.

作者信息

Bührle C P, Hackenthal E, Helmchen U, Lackner K, Nobiling R, Steinhausen M, Taugner R

出版信息

Lab Invest. 1986 Apr;54(4):462-72.

PMID:3515047
Abstract

Experimental hydronephrosis in mice has been studied with histological, ultrastructural, immunohistochemical, biochemical, and electrophysiological techniques to establish its value as a preparation for the investigation of glomerular microcirculation as well as the electrophysiological and biochemical properties of the renin-containing juxtaglomerular (JG) and vascular smooth muscle (VSM) cells of the afferent glomerular arteriole. During developing hydronephrosis the kidney parenchyma becomes progressively thinner as a result of tubular atrophy, being, after 12 weeks, a tissue sheet of about 200 micron in thickness. In this preparation, the renal arterial tree, in particular the glomerular arterioles, and also the glomeruli can be easily visualized. This permits intravital microscopic studies or direct visual identification of JG and VSM cells for microelectrode impalement. In spite of complete tubular atrophy, the vascular system is well preserved. Ultrastructurally, JG and VSM cells as well as the axon terminals innervating the vessels are intact. The same holds for the glomeruli except for a certain confluence of the podocyte foot processes and a thickening of the basal lamina. Renin immunostaining and kidney renin content in the hydronephrotic organ correspond to those in control kidneys. In addition, renin release from this preparation can be stimulated in a typical manner by isoproterenol and inhibited by angiotensin II, indicating that the receptors controling renin release and the secretory mechanism itself are still intact. Electrophysiological recordings from JG and VSM cells show a high membrane potential (-75 mv), and spontaneous depolarizing junction potentials, owing to transmitter release from the nerve terminals. Inhibitors of renin secretion, e.g. angiotensin II, depolarize both cell types, whereas stimulators such as isoproterenol do not change the membrane potential. We conclude that the hydronephrotic mouse kidney is a suitable model for in vitro studies of the electrophysiology and biochemistry of the media cells of the afferent arteriole, as well as for in vivo studies of glomerular microcirculation.

摘要

利用组织学、超微结构、免疫组织化学、生物化学和电生理技术对小鼠实验性肾积水进行了研究,以确定其作为研究肾小球微循环以及肾小球入球小动脉含肾素的球旁(JG)细胞和血管平滑肌(VSM)细胞的电生理和生化特性的一种制备模型的价值。在肾积水形成过程中,由于肾小管萎缩,肾实质逐渐变薄,12周后,成为厚度约200微米的组织薄片。在这种制备模型中,肾动脉树,特别是肾小球小动脉,以及肾小球都可以很容易地观察到。这使得可以进行活体显微镜研究或直接目视识别JG和VSM细胞以便进行微电极刺入。尽管肾小管完全萎缩,但血管系统保存完好。超微结构上,JG和VSM细胞以及支配血管的轴突终末都是完整的。肾小球除了足细胞足突有一定融合和基膜增厚外也是如此。肾积水器官中的肾素免疫染色和肾脏肾素含量与对照肾脏中的相当。此外,异丙肾上腺素能以典型方式刺激该制备模型释放肾素,而血管紧张素II则能抑制其释放,这表明控制肾素释放的受体和分泌机制本身仍然完好。对JG和VSM细胞的电生理记录显示膜电位较高(-75 mV),并且由于神经终末释放递质而出现自发去极化的连接电位。肾素分泌抑制剂,如血管紧张素II,会使两种细胞类型去极化,而异丙肾上腺素等刺激剂则不会改变膜电位。我们得出结论,肾积水小鼠肾脏是用于体外研究入球小动脉中层细胞电生理和生物化学以及体内研究肾小球微循环的合适模型。

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