Zimlichman R R, Chaimovitz C, Chaichenco Y, Goligorsky M, Rapoport J, Kaplanski J
Clin Sci (Lond). 1984 Aug;67(2):161-6. doi: 10.1042/cs0670161.
Studies were performed to evaluate the mechanism involved in the hypertension of moderate renal failure in partially (five-sixth) nephrectomized rats. Cardiac index (CI) was studied by means of the microsphere technique, and systemic vascular resistance (SVR) calculated from the mean arterial resistance MAP/CI, in four groups of experimental animals: (A) partially nephrectomized rats; (B) group A rats chronically treated with the calcium channel blocker verapamil; (C) sham-operated rats; (D) sham-operated rats treated with verapamil. The results demonstrate a significant increase in MAP in group A rats, which was due to a 72% increase in SVR as compared with groups C and D. In group B rats, MAP decreased significantly owing to a marked decrease in SVR (40%) as compared with group A. However, MAP remained higher in group B than in group C. The vascular responsiveness to noradrenaline was studied in group A, group C and group A rats after parathyroidectomy (group A1). An increased pressor responsiveness to noradrenaline was indicated by a shift of the noradrenaline dose-response curve to the left in group A rats as compared with group C rats. This change was corrected after partial nephrectomy. We conclude that hypertension in nephrectomized rats is due to an increase in SVR, and that an increased pressor responsiveness to catecholamines may play a role in this phenomenon. Furthermore, verapamil reduced the hypertension, and parathyroidectomy improved the abnormal sensitivity to noradrenaline in group A rats. These results raise the possibility that an abnormality in calcium metabolism, possibly due to secondary hyperparathyroidism, may be implicated in the hypertension of mildly uraemic rats.
开展了多项研究以评估部分（六分之五）肾切除大鼠中度肾衰竭高血压的发病机制。采用微球技术研究心脏指数（CI），并根据平均动脉压MAP/CI计算全身血管阻力（SVR），实验动物分为四组：（A）部分肾切除大鼠；（B）长期用钙通道阻滞剂维拉帕米治疗的A组大鼠；（C）假手术大鼠；（D）用维拉帕米治疗的假手术大鼠。结果显示，A组大鼠的MAP显著升高，这是由于与C组和D组相比，SVR增加了72%。B组大鼠的MAP显著降低，因为与A组相比，SVR显著降低（40%）。然而，B组的MAP仍高于C组。在A组、C组以及甲状旁腺切除后的A组大鼠（A1组）中研究了血管对去甲肾上腺素的反应性。与C组大鼠相比，A组大鼠去甲肾上腺素剂量-反应曲线左移，表明对去甲肾上腺素的升压反应性增加。部分肾切除后这种变化得到纠正。我们得出结论，肾切除大鼠的高血压是由于SVR增加所致，对儿茶酚胺升压反应性增加可能在这一现象中起作用。此外，维拉帕米降低了高血压，甲状旁腺切除改善了A组大鼠对去甲肾上腺素的异常敏感性。这些结果增加了一种可能性，即可能由于继发性甲状旁腺功能亢进导致的钙代谢异常可能与轻度尿毒症大鼠的高血压有关。
