Pecly I M D, Genelhu V, Francischetti E A
Hypertension Clinic-CLINEX, Rio de Janeiro State University, Rua Felipe Camarão, 82, Vila Isabel, Rio de Janeiro, CEP 20511-010, Brazil.
Int J Clin Pract. 2006 Oct;60(10):1198-203. doi: 10.1111/j.1742-1241.2006.01037.x.
The capacity to increase glomerular filtration rate in response to an acute oral protein load is known as the renal functional reserve; the loss of such capacity is used as a marker of hyperfiltration. This physiological response in obese hypertensives is not yet fully understood. We aimed to study the interdependent effects of obesity and hypertension on renal reserve, taking into account renal kallikrein and nitric oxide in the modulation of that parameter. Fourteen obese hypertensives (mean age, 50.5 +/- 0.9 years) and nine lean hypertensives (mean age, 50.6 +/- 2.7 years) were evaluated. Renal haemodynamics and the levels of serum nitric oxide and urinary kallikrein were assessed at baseline and after a protein load (1 g/kg of body weight). An increase in the following parameters was observed when comparing obese and lean hypertensives: basal glomerular filtration rate; renal plasma flow; and urinary kallikrein and nitric oxide levels (129.2 +/- 2.9 vs. 101.4 +/- 3.4 ml/min/1.73 m2; 587.5 +/- 18.2 vs. 502.8 +/- 16.7 ml/min/1.73 m2; 0.120 +/- 0.02 vs. 0.113 +/- 0.02 mU/ml; 23.2 +/- 0.8 vs. 19.5 +/- 1.2 mmol/ml, respectively). The renal reserve was lower in obese hypertensives when compared with that of lean hypertensives (4.1 +/- 0.5 vs. 11.8 +/- 0.8 ml/min, p < 0.005). After a protein load, contrasting with the lean group, inability to elevate the nitric oxide serum levels and a lower increase in urinary kallikrein were observed in the obese group. These data suggest that obese hypertensives lose renal reserve earlier in the evolution to renal dysfunction. This may be due to the defective modulation of renal vasodilatation mechanisms by renal kallikrein and nitric oxide production.
因急性口服蛋白质负荷而增加肾小球滤过率的能力被称为肾功能储备；这种能力的丧失被用作超滤的一个标志。肥胖高血压患者的这种生理反应尚未完全被理解。我们旨在研究肥胖和高血压对肾储备的相互依存效应，同时考虑肾激肽释放酶和一氧化氮在该参数调节中的作用。对14名肥胖高血压患者（平均年龄50.5±0.9岁）和9名瘦高血压患者（平均年龄50.6±2.7岁）进行了评估。在基线和蛋白质负荷（1 g/kg体重）后评估肾血流动力学以及血清一氧化氮水平和尿激肽释放酶水平。比较肥胖和瘦高血压患者时观察到以下参数增加：基础肾小球滤过率；肾血浆流量；以及尿激肽释放酶和一氧化氮水平（分别为129.2±2.9 vs. 101.4±3.4 ml/min/1.73 m²；587.5±18.2 vs. 502.8±16.7 ml/min/1.73 m²；0.120±0.02 vs. 0.113±0.02 mU/ml；23.2±0.8 vs. 19.5±1.2 mmol/ml）。与瘦高血压患者相比，肥胖高血压患者的肾储备较低（4.1±0.5 vs. 11.8±0.8 ml/min，p<0.005）。蛋白质负荷后，与瘦组形成对比的是，肥胖组出现无法提高血清一氧化氮水平以及尿激肽释放酶增加较少的情况。这些数据表明，肥胖高血压患者在向肾功能不全演变过程中更早地丧失肾储备。这可能是由于肾激肽释放酶和一氧化氮产生对肾血管舒张机制的调节缺陷所致。
