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Metaplastic and mitotic activity of the ischemic (endocrine) kidney in experimental renal hypertension.

机译:实验性肾性高血压中缺血性(内分泌)肾脏的化生和有丝分裂活性。

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摘要

Partial ligation of the aorta between the renal arteries in the rat induces malignant hypertension, metaplasia of smooth-muscle cells of arterioles and arteries into juxtaglomerular cells, and a complex series of events in tubular cells at all levels of the ischemic kidney. The tubular cells of the outer cortex, particularly the proximal convoluted cells, show a very rapid and progressive simple atrophy. In contrast, necrosis of individual cells is followed by mitotic activity in atrophic tubular cells of the inner cortex, medulla, and papilla. Subsequently, polyploidy and hyperplasia occur in the inner cortex. At the same time, hypertrophy of the protein-synthesizing apparatus and an increase in protein, DNA, and RNA, followed by a decrease in the protein content, are seen in the tubular cells of the inner cortex. In the medulla and papilla, necrosis of individual cells proceeds side by side with waves of mitotic activity. These events take place, albeit to a lesser degree, even in cases of very mild renal ischemia. While they may by unrelated to hypertension, these changes are probably involved in the increase in hydrolytic enzyme activity characteristic of the ischemic renal cortex.
机译:大鼠肾动脉之间的主动脉部分结扎可诱发恶性高血压,小动脉和动脉的平滑肌细胞化生为近肾小球细胞,以及缺血肾各个水平的肾小管细胞发生一系列复杂的事件。外部皮质的管状细胞,特别是近端的回旋细胞,显示出非常迅速和进行性的简单萎缩。相比之下,单个细胞的坏死随后是内皮层,髓质和乳头的萎缩性管状细胞中的有丝分裂活性。随后,在内层皮层中发生多倍体和增生。同时,在内皮的肾小管细胞中可见到蛋白质合成装置的肥大和蛋白质,DNA和RNA的增加,随后蛋白质含量的减少。在髓质和乳头中,单个细胞的坏死与有丝分裂活动的波并排进行。即使在轻度肾脏缺血的情况下,这些事件的发生程度也有所降低,尽管程度较小。尽管它们可能与高血压无关,但这些变化可能与缺血性肾皮质的水解酶活性特征增加有关。

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