Tikkanen I, Fyhrquist F, Miettinen A, Törnroth T
Acta Pathol Microbiol Scand A. 1980 Jul;88(4):241-50. doi: 10.1111/j.1699-0463.1980.tb02492.x.
In order to explore immunological features of hypertension, we studied autologous immune complex nephritis (Heymann nephritis) combined with DOCA-NaCl treatment. This combination resulted in hypertension and increased heart weight whereas DOCA-NaCl treatment alone induced only a slight elevation of blood pressure and a moderate increase in heart weight. Nephritic rats without DOCA-NaCl load remained normotensive, their heart weights being comparable to those of controls. This new model of hypertension was neither characterized by azotemia nor by reduced renal excretory capacity. Hypertension was not renin-angiotensin-dependent. DOCA-NaCl treatment accelerated the development of proteinuria. In the hypertensive rats, systolic blood pressure to daily urinary protein excretion. Renal histopathology revealed changes resembling those of malignant nephrosclerosis. Immunohistology and electron microscopy showed a typical membranous glomerulonephritis in all immunized animals. It was concluded that immune complex disease of the Heymann nephritis type may interfere with normal hemodynamic adaptation to hypervolemic sodium load, resulting in hypertension.
为了探究高血压的免疫学特征，我们研究了自体免疫复合物性肾炎（海曼肾炎）联合去氧皮质酮-氯化钠治疗的情况。这种联合治疗导致了高血压和心脏重量增加，而单独使用去氧皮质酮-氯化钠治疗仅引起血压轻度升高和心脏重量适度增加。未接受去氧皮质酮-氯化钠负荷的肾炎大鼠血压正常，其心脏重量与对照组相当。这种新的高血压模型既没有氮质血症的特征，也没有肾脏排泄能力降低的特征。高血压不依赖肾素-血管紧张素。去氧皮质酮-氯化钠治疗加速了蛋白尿的发展。在高血压大鼠中，收缩压与每日尿蛋白排泄量相关。肾脏组织病理学显示出类似于恶性肾硬化的变化。免疫组织学和电子显微镜检查显示，所有免疫动物均存在典型的膜性肾小球肾炎。研究得出结论，海曼肾炎型免疫复合物疾病可能会干扰对高血容量钠负荷的正常血流动力学适应，从而导致高血压。
