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肾小球肥大加速大鼠高血压性肾小球损伤。

Glomerular hypertrophy accelerates hypertensive glomerular injury in rats.

作者信息

Miller P L, Rennke H G, Meyer T W

机构信息

Department of Medicine, Stanford University, California 94305.

出版信息

Am J Physiol. 1991 Sep;261(3 Pt 2):F459-65. doi: 10.1152/ajprenal.1991.261.3.F459.

DOI:10.1152/ajprenal.1991.261.3.F459
PMID:1887907
Abstract

Micropuncture and morphological studies were performed in four groups of rats that received subcutaneous infusions of saline or angiotensin II (ANG II) for 8 wk. Group 1 rats received saline; group 2 rats were subjected to uninephrectomy and then received saline; group 3 rats received ANG II (100 ng/min); and group 4 rats were subjected to uninephrectomy and then received ANG II (50 ng/min). In comparison with group 1 rats, group 2 rats exhibited no increase in mean arterial pressure (MAP) (group 2, 102 +/- 6 mmHg; group 1, 104 +/- 10 mmHg) or glomerular capillary pressure (PGC) (group 2, 56 +/- 3 mmHg; group 1, 55 +/- 4 mmHg). In the absence of glomerular hypertension, an increase in glomerular volume (VG) was not associated with glomerular sclerosis in group 2 rats. In contrast to group 2 rats, group 3 rats exhibited increases in MAP (161 +/- 13 mmHg) and PGC (70 +/- 7 mmHg) without any increase in VG. Glomerular hypertension was associated with development of increased albuminuria and glomerular sclerosis in group 3. Group 4 rats exhibited increases in MAP (157 +/- 18 mmHg), PGC (69 +/- 6 mmHg), and VG. These rats also developed glomerular sclerosis and significantly more albuminuria than would have been expected from simple combination of effects of uninephrectomy and ANG II infusion. Additional morphological studies were performed in two groups of rats that received ANG II for 12 wk. Over this period, uninephrectomized group 6 rats infused with ANG II (50 ng/min) developed markedly greater albuminuria and glomerular sclerosis than intact group 5 rats infused with ANG II (100 ng/min).(ABSTRACT TRUNCATED AT 250 WORDS)

摘要

对四组大鼠进行了微穿刺和形态学研究,这四组大鼠皮下输注生理盐水或血管紧张素II(ANG II),为期8周。第1组大鼠输注生理盐水;第2组大鼠接受单侧肾切除,然后输注生理盐水;第3组大鼠输注ANG II(100 ng/分钟);第4组大鼠接受单侧肾切除,然后输注ANG II(50 ng/分钟)。与第1组大鼠相比,第2组大鼠的平均动脉压(MAP)(第2组,102±6 mmHg;第1组,104±10 mmHg)和肾小球毛细血管压(PGC)(第2组,56±3 mmHg;第1组,55±4 mmHg)均未升高。在无肾小球高血压的情况下,第2组大鼠肾小球体积(VG)的增加与肾小球硬化无关。与第2组大鼠相反,第3组大鼠的MAP(161±13 mmHg)和PGC(70±7 mmHg)升高,而VG未增加。第3组中,肾小球高血压与蛋白尿增加和肾小球硬化的发展相关。第4组大鼠的MAP(157±18 mmHg)、PGC(69±6 mmHg)和VG均升高。这些大鼠还出现了肾小球硬化,蛋白尿也明显多于仅由单侧肾切除和ANG II输注的综合作用所预期的水平。对另外两组输注ANG II 12周的大鼠进行了额外的形态学研究。在此期间,接受ANG II(50 ng/分钟)输注的单侧肾切除的第6组大鼠,比接受ANG II(100 ng/分钟)输注的完整第5组大鼠出现了明显更多的蛋白尿和肾小球硬化。(摘要截短于250字)

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