Winternitz S R, Katholi R E, Oparil S
J Clin Invest. 1980 Nov;66(5):971-8. doi: 10.1172/JCI109966.
Neurogenic factors and, in particular, enhanced renal sympathetic tone, have been implicated in the pathogenesis of hypertension in the spontaneously hypertensive rat of the Okamoto strain. To examine the hypothesis that the renal sympathetic nerves contribute to the development and maintenance of hypertension by causing urinary sodium retention, 7-wk-old (early hypertensive) and 18-wk-old (established hypertensive) male spontaneously hypertensive rats were subjected to bilateral renal denervation and compared with sham-operated controls. In 7-wk-old animals renal denervation delayed the onset and slowed the rate of development of hypertension. These alterations were associated with a significantly greater fractional excretion of sodium (percentage of sodium intake excreted) during the first 3 wk after denervation. Blood pressure 2 wk after surgery was 169+/-3.5 (sham) vs. 150+/-2.4 mm Hg (denervated) (P < 0.001), corresponding to fractional sodium excretions of 65+/-1.3% (sham) vs. 80+/-2.3% (denervated) (P < 0.001). By the 5th wk after surgery, at which time an increase in renal norepinephrine content of denervated animals suggested reinnervation, blood pressures in the two groups converged (sham, 199+/-6.5 mm Hg vs. denervated 180+/-3.5 mm Hg, NS) and there was no difference in sodium excretion (sham, 77+/-2.5% vs. denervated 79+/-2.3%). Plasma and kidney renin activity of denervated animals did not differ significantly from that of sham-operated controls. In 18-wk-old rats renal denervation did not alter blood pressure or urinary sodium excretion. These data indicate that the renal sympathetic nerves contribute to the development of hypertension in the spontaneously hypertensive rat in part by causing enhanced sodium retention. Once hypertension is established the renal nerves do not play a significant role in the maintenance of increased blood pressure.
神经源性因素，尤其是肾交感神经张力增强，与冈本品系自发性高血压大鼠的高血压发病机制有关。为检验肾交感神经通过导致尿钠潴留促进高血压发生和维持这一假说，将7周龄（早期高血压）和18周龄（已患高血压）的雄性自发性高血压大鼠进行双侧肾去神经支配，并与假手术对照组进行比较。在7周龄动物中，肾去神经支配延迟了高血压的发作并减缓了其发展速度。这些改变与去神经支配后的前3周内钠的分数排泄率（排泄的钠摄入量百分比）显著增加有关。术后2周时，血压分别为169±3.5（假手术组）和150±2.4 mmHg（去神经支配组）（P<0.001），对应的钠分数排泄率分别为65±1.3%（假手术组）和80±2.3%（去神经支配组）（P<0.001）。术后第5周时，去神经支配动物肾去甲肾上腺素含量增加提示有神经再支配，两组血压趋于一致（假手术组，199±6.5 mmHg；去神经支配组，180±3.5 mmHg，无显著性差异），钠排泄也无差异（假手术组，77±2.5%；去神经支配组，79±2.3%）。去神经支配动物的血浆和肾脏肾素活性与假手术对照组相比无显著差异。在18周龄大鼠中，肾去神经支配未改变血压或尿钠排泄。这些数据表明，肾交感神经部分通过导致钠潴留增加促进自发性高血压大鼠高血压的发生。一旦高血压形成，肾神经在维持血压升高中不起重要作用。
