Wilson S K, Solez K, Heptinstall R H
Am J Pathol. 1980 Nov;101(2):303-18.
The concept has been advanced that malignant hypertension is precipitated in the rat with renal hypertension by a sudden loss of sodium in the urine. In order to test this hypothesis modest degrees of hypertension were produced in Holtzman rats by the application of a silver clip to one renal artery, not touching the opposite kidney. When the systolic blood pressure reached a level between 160 and 180 mm Hg, loss of sodium and water was induced by the administration of furosemide, given either orally over a 7-day period, or by 3 intramuscular injections over a 24-hour period. Sodium and water balance studies, blood pressure determinations, histologic assessment of blood vessels in the nonclipped kidney, and measurement of activity of the juxtaglomerular apparatus were carried out in these 2 groups and appropriate control animals. It was found that in spite of a considerable natriuresis and diuresis in furosemide-treated animals, there was neither a significant increase in the blood pressure nor development of more severe vascular lesions in the nonclipped kidney than in the kidneys of control animals.
有一种观点认为，肾性高血压大鼠因尿液中钠的突然流失而引发恶性高血压。为了验证这一假设，通过对霍尔茨曼大鼠的一侧肾动脉施加银夹（不触及对侧肾脏），使其产生轻度高血压。当收缩压达到160至180毫米汞柱之间时，通过口服呋塞米7天或在24小时内进行3次肌肉注射来诱导钠和水的流失。对这两组动物以及适当的对照动物进行了钠和水平衡研究、血压测定、未夹闭肾脏血管的组织学评估以及肾小球旁器活性的测量。结果发现，尽管呋塞米治疗的动物出现了大量的尿钠排泄和利尿，但与对照动物的肾脏相比，未夹闭肾脏的血压既没有显著升高，也没有出现更严重的血管病变。
