de Magalhães Sartim Ricardo, Fantinato Menegon Leonardo, de Almeida Amanda Roberta, Rocha Gontijo José Antonio, Aline Boer Patricia
Laboratórios de Metabolismo Hidro-Salino, Departamento de Clinica Médica, Núcleo de Medicina e Cirurgia Experimental, Faculdade de Ciências Médicas, Universidade Estadual de Campinas, Campinas Uniararas, SP, Brazil.
Ren Fail. 2006;28(6):501-7. doi: 10.1080/08860220600779058.
The role of the kidney in the control of blood pressure has been convincingly demonstrated by several studies. Recent evidence has suggested that subtle acquired tubulointerstitial injury may cause a defect in sodium excretion function, thus leading to salt-sensitive hypertension. There are no reports, however, examining the effect of experimental chronic pyelonephritis on renal sodium handling and arterial pressure. Thus, to examine the influence of salt intake and unilateral nephrectomy, unanesthetized, unrestrained rats were randomly assigned to one of two separate groups: sham-operated rats (CO) or chronic unilateral pyelonephritic rats (CP). After twenty one days, the pyelonephritic group was subdivided in two: one subgroup continued with water intake (CPw), while the other was changed to 0.9% NaCl intake (CPs), like the control group (COs). After seven days, all rats were submitted to unilateral nephrectomy of the left normal kidney. Data presented herein show that chronic pyelonephritis produced an increase in mean arterial pressure (CO: 121.4 +/- 1.0 mmHg to CP: 127.0 +/- 0.9 mmHg, p = 0.000) that was enhanced by saline ingestion (COs: 121.6 +/- 1.4 mmHg; CPw: 127.0 +/- 1.8 mmHg; CPs: 132.1 +/- 1.2 mmHg, p = 0.000) and further aggravated by unilateral nephrectomy (CO: 125.2 +/- 2.6 mmHg; CPw: 127.5 +/- 0.9 mmHg; CPs: 139.2 +/- 1.1 mmHg, p = 0.000). Unchanged blood pressure measurements (120.2 +/- 2.3 mmHg) were observed beyond 21 days in control rats maintained on water regimen when compared with saline-drinking groups. These changes in mean arterial pressure were observed despite an increased fractional sodium excretion in the CPs group compared to the other groups before uninephrectomy (COs: 0.125 +/- 0.025%; CPw: 0.045 +/- 0.013%; CPs: 0.292 +/- 0.046%; p = 0.000), as compared to CPw after uninephrectomy (COs: 0.249 +/- 0.077%; CPw: 0.062 +/- 0.011%; CPs: 0.363 +/- 0.195%, p = 0.019). In addition, it was shown that daily liquid intake was higher in CPs than in CPw but similar to COs, both before uninephrectomy (COs: 42.8 +/- 2.6 ml/d; CPw: 34.3 +/- 3.5 ml/d; CPs: 51.8 +/- 3.7 ml/d, p = 0.006) and after uninephrectomy (COs: 40.9 +/- 5.5 ml/d; CPw: 33.8 +/- 1.4 ml/d; CPs: 53.0 +/- 3.5 ml/d, p = 0.004). The current data suggest that chronic pyelonephritis promotes an inability of renal tubules to handle sodium excretion when exposed to sodium overload and aggravated by uninephrectomy, thus constituting a model for salt-sensitive hypertension.
多项研究令人信服地证明了肾脏在血压控制中的作用。最近的证据表明，轻微的后天性肾小管间质损伤可能导致钠排泄功能缺陷，从而引发盐敏感性高血压。然而，尚无研究探讨实验性慢性肾盂肾炎对肾脏钠处理及动脉血压的影响。因此，为研究盐摄入和单侧肾切除的影响，将未麻醉、未受限制的大鼠随机分为两组：假手术大鼠（CO）和慢性单侧肾盂肾炎大鼠（CP）。21天后，将肾盂肾炎组再分为两个亚组：一个亚组继续饮水（CPw），另一个亚组改为摄入0.9%氯化钠（CPs），与对照组（COs）相同。7天后，所有大鼠均接受左侧正常肾脏的单侧肾切除术。本文提供的数据表明，慢性肾盂肾炎使平均动脉压升高（CO：121.4±1.0 mmHg至CP：127.0±0.9 mmHg，p = 0.000），摄入盐水会使其进一步升高（COs：121.6±1.4 mmHg；CPw：127.0±1.8 mmHg；CPs：132.1±1.2 mmHg，p = 0.000），单侧肾切除会使其进一步加重（CO：125.2±2.6 mmHg；CPw：127.5±0.9 mmHg；CPs：139.2±1.1 mmHg，p = 0.000）。与饮用盐水的组相比，维持饮水方案的对照大鼠在21天后血压测量值无变化（120.2±2.3 mmHg）。尽管在单侧肾切除术前，CPs组的钠排泄分数高于其他组（COs：0.125±0.025%；CPw：0.045±0.013%；CPs：0.292±0.046%；p = 0.000），但与单侧肾切除术后的CPw组相比（COs：0.249±0.077%；CPw：0.062±0.011%；CPs：0.363±0.195%，p = 0.019），仍观察到平均动脉压的这些变化。此外，研究表明，在单侧肾切除术前（COs：42.8±2.6 ml/d；CPw：34.3±3.5 ml/d；CPs：51.8±3.7 ml/d，p = 0.006）和单侧肾切除术后（COs：40.9±5.5 ml/d；CPw：33.8±1.4 ml/d；CPs：53.0±3.5 ml/d，p = 0.004），CPs组的每日液体摄入量均高于CPw组，但与COs组相似。目前的数据表明，慢性肾盂肾炎会导致肾小管在钠负荷过重时无法处理钠排泄，单侧肾切除会使其加重，从而构成盐敏感性高血压的模型。
