Vari R C, Freeman R H, Davis J O, Sweet W D
Am J Physiol. 1986 Feb;250(2 Pt 2):H189-94. doi: 10.1152/ajpheart.1986.250.2.H189.
This study examined the role of the renal nerves in both the maintenance and developmental phases of hypertension produced by sodium restriction in one-kidney rats. Results indicate that mild hypertension is sustained through 6 wk after unilateral nephrectomy in rats fed a sodium-deficient diet, with the greatest increase in systolic blood pressure occurring within the first 2 wk. Six weeks after nephrectomy, renal denervation was performed in the sodium-restricted, hypertensive rats, and the blood pressure returned to normotensive levels. Plasma renin activity (PRA) was elevated fourfold after 6 wk of sodium restriction and was unchanged by renal denervation. In another series of experiments that examined the development of hypertension in this experimental model, contralateral renal denervation was performed at the time of nephrectomy, and this prevented the subsequent development of hypertension. PRA was significantly attenuated in these low-sodium, renal-denervated rats that failed to become hypertensive when compared with PRA in hypertensive low-sodium, sham-denervated rats. Kidney norepinephrine content was reduced by 96% after renal denervation in both phases of the hypertension. These data demonstrate that intact renal nerves are necessary for both the development and maintenance of mild hypertension after sodium restriction in one-kidney rats. The pressor contribution of the renal nerves to the hypertension in this experimental model appears to be related, at least in part, to the activation of the renin-angiotensin pressor mechanism.
本研究探讨了肾神经在一侧肾脏切除的大鼠因限钠所致高血压的维持和发展阶段所起的作用。结果表明,在喂食缺钠饮食的大鼠中,单侧肾切除术后6周内轻度高血压持续存在,收缩压在最初2周内升高最为明显。肾切除术后6周,对限钠的高血压大鼠进行肾去神经支配,血压恢复到正常水平。限钠6周后血浆肾素活性(PRA)升高四倍,肾去神经支配对其无影响。在另一系列研究该实验模型中高血压发展情况的实验中,在肾切除时对侧肾去神经支配,这可防止随后高血压的发展。与高血压低钠假去神经支配大鼠的PRA相比,这些未发生高血压的低钠肾去神经支配大鼠的PRA显著降低。在高血压的两个阶段,肾去神经支配后肾脏去甲肾上腺素含量均降低96%。这些数据表明,完整的肾神经对于一侧肾脏切除的大鼠限钠后轻度高血压的发展和维持均是必需的。在该实验模型中,肾神经对高血压的升压作用似乎至少部分与肾素 - 血管紧张素升压机制的激活有关。