Kimura K, Tojo A, Hirata Y, Matsuoka H, Sugimoto T
Second Department of Internal Medicine, Faculty of Medicine, University of Tokyo, Japan.
J Lab Clin Med. 1993 Sep;122(3):273-83.
Renal arteriolar diameters were measured by using vascular casts in the remnant kidneys of subtotally nephrectomized rats. Two weeks after nephrectomy, both afferent and efferent arterioles were dilated, with development of glomerular hypertrophy. Thirteen weeks after nephrectomy, the afferent arteriole was dilated further, while the efferent arterioles became constricted. Glomerular hypertrophy was augmented. At this stage, the systemic pressure was elevated, with development of marked glomerular sclerosis. Throughout the experiment, captopril lowered the systemic pressure, suppressed glomerular hypertrophy, and limited glomerular damage. Both the afferent and efferent arterioles were dilated further. Changes in the arteriolar diameters and the systemic blood pressure suggested that elevated glomerular pressure existed in the remnant kidney and did not exist in the captopril-treated remnant kidney throughout the experiment. Hydralazine and trichloromethiazide therapy lowered the systemic pressure and maintained the arteriolar diameters and glomerular size at normal levels. However, at the late stage, afferent and efferent arterioles were dilated, with development of glomerular hypertrophy and severe glomerular sclerosis. The results suggested that elevated glomerular pressure was involved in development of glomerular sclerosis. However, factors other than hemodynamics should be considered in the pathogenesis of glomerular sclerosis. A direct causal relationship between glomerular hypertrophy and glomerular damage was not shown because captopril ultimately limited glomerular sclerosis despite glomerular hypertrophy at the early stage, and hydralazine and trichloromethiazide therapy did not ultimately ameliorate the glomerular sclerosis despite normal glomerular size at the early stage.
通过使用血管铸型测量了次全肾切除大鼠残余肾脏的肾小动脉直径。肾切除术后两周，入球小动脉和出球小动脉均扩张，伴有肾小球肥大的发展。肾切除术后13周，入球小动脉进一步扩张，而出球小动脉则收缩。肾小球肥大加剧。在此阶段，全身血压升高，伴有明显的肾小球硬化的发展。在整个实验过程中，卡托普利降低了全身血压，抑制了肾小球肥大，并限制了肾小球损伤。入球小动脉和出球小动脉均进一步扩张。小动脉直径和全身血压的变化表明，残余肾脏中存在肾小球压力升高，而在整个实验过程中卡托普利治疗的残余肾脏中不存在这种情况。肼屈嗪和氢氯噻嗪治疗降低了全身血压，并将小动脉直径和肾小球大小维持在正常水平。然而，在后期，入球小动脉和出球小动脉扩张，伴有肾小球肥大和严重的肾小球硬化的发展。结果表明，肾小球压力升高参与了肾小球硬化的发展。然而，在肾小球硬化的发病机制中应考虑血流动力学以外的因素。未显示肾小球肥大与肾小球损伤之间存在直接因果关系，因为尽管早期存在肾小球肥大，但卡托普利最终限制了肾小球硬化，而尽管早期肾小球大小正常，但肼屈嗪和氢氯噻嗪治疗最终并未改善肾小球硬化。
