Carlström M, Wåhlin N, Skøtt O, Persson A E G
Department of Medical Cell Biology, Division of Integrative Physiology, University of Uppsala, Uppsala, Sweden.
Acta Physiol (Oxf). 2007 Jan;189(1):67-75. doi: 10.1111/j.1748-1716.2006.01625.x.
The incidence of hydronephrosis due to ureteropelvic junction obstruction is approx. 0.5%. During the last decade, the management of non-symptomatic hydronephrosis has become much more conservative, but the long-term physiological consequences of this policy are not clear. Previously, we have shown that animals with chronic partial unilateral ureteral obstruction develop salt-sensitive hypertension. In this study, the effects of ipsilateral and contralateral nephrectomy and ureterovesicostomy on blood pressure were studied in hydronephrotic animals.
Partial unilateral ureteral obstruction was created in 3-week-old male Sprague-Dawley rats and blood pressure was measured telemetrically 4-6 weeks later during a normal and high salt diet before and after uninephrectomy or ureterovesicostomy. Plasma samples for renin assay were collected during both diets before and after ipsilateral nephrectomy.
All hydronephrotic animals developed salt-sensitive hypertension, of different degrees. Before nephrectomy the plasma renin concentration was significantly higher in the hydronephrotic animals than in controls (160 +/- 15 microGU mL(-1) vs. 96 +/- 12 microGU mL(-1), respectively), but after the ipsilateral nephrectomy no differences were found between the groups. In the hydronephrotic animals both ipsilateral nephrectomy and ureterovesicostomy reduced the blood pressure and salt-sensitivity but the former still differed significantly from the controls. In contralaterally, nephrectomized hydronephrotic animals the salt-sensitive hypertension became more pronounced.
Hydronephrosis in rats causes salt-sensitive hypertension that can be markedly reduced by removing the hydronephrotic kidney or relieving the obstruction by ureterovesicostomy. The mechanisms appear to be intrarenal and primarily located in the diseased kidney, but a secondary mechanism is also present.
肾盂输尿管连接部梗阻所致肾积水的发病率约为0.5%。在过去十年中，无症状肾积水的治疗变得更加保守，但该策略的长期生理后果尚不清楚。此前，我们已表明，患有慢性部分单侧输尿管梗阻的动物会出现盐敏感性高血压。在本研究中，我们研究了同侧和对侧肾切除术以及输尿管膀胱吻合术对肾积水动物血压的影响。
在3周龄雄性Sprague-Dawley大鼠中制造部分单侧输尿管梗阻，并在4-6周后通过遥测技术在正常和高盐饮食期间测量肾切除术或输尿管膀胱吻合术前后的血压。在同侧肾切除术前后的两种饮食期间收集用于肾素测定的血浆样本。
所有肾积水动物均出现不同程度的盐敏感性高血压。肾切除术前，肾积水动物的血浆肾素浓度显著高于对照组（分别为160±15微GU/mL对96±12微GU/mL），但同侧肾切除术后两组之间未发现差异。在肾积水动物中，同侧肾切除术和输尿管膀胱吻合术均降低了血压和盐敏感性，但前者仍与对照组有显著差异。在对侧肾切除的肾积水动物中，盐敏感性高血压变得更加明显。
大鼠肾积水会导致盐敏感性高血压，通过切除积水肾或通过输尿管膀胱吻合术解除梗阻可显著降低血压。其机制似乎是肾内性的，主要位于患病肾脏，但也存在次要机制。
