Sanai T, Kimura G
Department of Medicine, National Cardiovascular Center, Osaka, Japan.
J Lab Clin Med. 1996 Jul;128(1):89-97. doi: 10.1016/s0022-2143(96)90117-1.
It has been postulated that glomerular capillary pressure is elevated in sodium-sensitive types of hypertension. In addition, the presence or absence of renal function reserve, in response to a chronic protein load, is thought to be useful in predicting the existence of glomerular hypertension. Intrarenal hemodynamic parameters in the sodium-sensitive type of essential hypertension were therefore calculated by analyzing the pressure-natriuresis curve, and the preservation of renal function reserve was evaluated. Fifteen patients with essential hypertension were maintained on a normal sodium diet for 1 week and a low-sodium diet for a second week in study 1. This protocol was repeated for low and high protein intake in 8 patients in study 2. Subjects in study 1 whose mean arterial pressure was reduced by more than 10% by sodium restriction were considered sodium sensitive (n = 7), with the remaining patients classified as non-sodium sensitive (n = 8). There were no significant differences in mean arterial pressure (125 +/- 2 mm Hg), glomerular filtration rate (80 +/- 3 ml/min), or renal plasma flow rate (355 +/- 24 ml/min) on the normal sodium diet between sodium-sensitive and non-sodium-sensitive patients. Glomerular capillary pressure (59 +/- 2 mm Hg vs 47 +/- 1 mm Hg, p < 0.0002) was estimated to be elevated in sodium-sensitive patients relative to that in non-sodium-sensitive patients, whereas the whole kidney ultrafiltration coefficient of glomerular capillary walls (0.068 +/- 0.009 (ml/sec)/mm Hg vs 0.221 +/- 0.042 (ml/sec)/mm Hg, p < 0.005) was decreased. Chronic protein loading increased both glomerular filtration and renal plasma flow rates in study 2. Although the sodium sensitivity of blood pressure showed no significant correlation with the increase in either glomerular filtration or renal plasma flow rate, it showed a weak negative correlation with the increase in filtration fraction (r = -0.69, p < 0.06), which is the ratio of the two rates. Taken together, these results suggest that glomerular capillary pressure is elevated and renal function reserve is impaired in patients with sodium-sensitive essential hypertension.
据推测，在钠敏感性高血压类型中，肾小球毛细血管压力会升高。此外，人们认为，针对慢性蛋白质负荷，肾功能储备的存在与否有助于预测肾小球高血压的存在。因此，通过分析压力-利钠曲线计算钠敏感性原发性高血压患者的肾内血流动力学参数，并评估肾功能储备的维持情况。在研究1中，15例原发性高血压患者先维持正常钠饮食1周，然后在第二周改为低钠饮食。在研究2中，8例患者针对低蛋白和高蛋白摄入量重复了该方案。在研究1中，平均动脉压因限钠而降低超过10%的受试者被认为是钠敏感型（n = 7），其余患者被归类为非钠敏感型（n = 8）。在正常钠饮食情况下，钠敏感型和非钠敏感型患者之间的平均动脉压（125±2 mmHg）、肾小球滤过率（80±3 ml/min）或肾血浆流量（355±24 ml/min）没有显著差异。相对于非钠敏感型患者，钠敏感型患者的肾小球毛细血管压力估计升高（59±2 mmHg对47±1 mmHg，p < 0.0002），而肾小球毛细血管壁的全肾超滤系数降低（0.068±0.009（ml/秒）/mmHg对0.221±0.042（ml/秒）/mmHg，p < 0.005）。在研究2中，慢性蛋白质负荷增加了肾小球滤过率和肾血浆流量。虽然血压的钠敏感性与肾小球滤过率或肾血浆流量的增加均无显著相关性，但与滤过分数的增加呈弱负相关（r = -0.69，p < 0.06），滤过分数是这两个速率的比值。综上所述，这些结果表明，钠敏感性原发性高血压患者的肾小球毛细血管压力升高，且肾功能储备受损。
