Freeman R H, Davis J O, Watkins B E
Am J Physiol. 1977 Oct;233(4):F278-81. doi: 10.1152/ajprenal.1977.233.4.F278.
The theory of whole body autoregulation to explain the pathogenesis of experimental renal hypertension states that hypertension is initiated in response to an early increase in salt and water retention and a subsequent elevation of the cardiac output. This hypothesis was evaluated in the present study. Dogs (n,5) were made hypertensive by wrapping the left kidney in cellophane and removing the contralateral kidney 3 wk later. One week prior to right nephrectomy, the dogs were volume depleted by placing them on a low sodium intake (less than 3 meq of sodium/day) and giving them a mercurial diuretic for the first 3 days of the diet. This superimposed sodium depletion (negative sodium balance of 137 +/- 17 meq) increased plasma renin activity 3-5 times but did not change arterial pressure or heart rate. Within 2 days after nephrectomy, the mean arterial pressure increased from the control level of 105 +/- 1 to 135 +/- 6 mmHg (P less than 0.005) and pressure remained elevated throughout an additional 4-wk period in which volume depletion was enforced. The present study suggests, therefore, that initial blood volume expansion with such possible consequences as elevated cardiac output are not essential to the pathogenesis of experimental renal hypertension.
用于解释实验性肾性高血压发病机制的全身自动调节理论指出，高血压是对早期盐和水潴留增加以及随后心输出量升高的反应而引发的。本研究对这一假说进行了评估。通过用玻璃纸包裹左肾并在3周后切除对侧肾脏使5只狗患高血压。在右肾切除术前1周，通过让狗摄入低钠饮食（每天钠摄入量少于3毫当量）并在饮食的前3天给予汞利尿剂，使狗的血容量减少。这种叠加的钠缺乏（负钠平衡为137±17毫当量）使血浆肾素活性增加了3至5倍，但未改变动脉血压或心率。肾切除术后2天内，平均动脉压从105±1 mmHg的对照水平升至135±6 mmHg（P<0.005），并且在另外4周强制血容量减少的期间内血压一直保持升高。因此，本研究表明，初始血容量扩张及其可能导致的心输出量升高对于实验性肾性高血压的发病机制并非必不可少。
