Renal autoregulation and passive pressure-flow relationships in diabetes and hypertension
Renal autoregulation and passive pressure-flow relationships in diabetes and hypertension
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DOI：
10.1152/ajprenal.00727.2009
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发表时间：
2010-10-01
影响因子：
4.2
通讯作者：
Endre, Z. H.
中科院分区：
文献类型：
--
作者：
Hill, J. V.;Findon, G.;Endre, Z. H.
Hill JV，Findon G，Appelhoff RJ，Endre ZH.糖尿病和高血压患者的肾脏自动调节和被动压力-流量关系。美国肾脏生理学杂志299：F837-F844，2010年。首次发表于2010年7月21日; doi：10.1152/ajprenal.00727.2009。我们研究了糖尿病和高血压大鼠模型的离体灌注肾脏的血流动力学。在血管紧张素II（pEC 50）或罂粟碱（0.1 mM）的存在下，分别使用阶梯式压力斜坡测量自动调节和被动血管反应。将雄性糖尿病杂合子m（Ren 2）27大鼠与三个雄性对照组进行比较：非糖尿病、血压正常的Sprague-Dawley（SD）大鼠;非糖尿病、高血压杂合子m（Ren 2）27大鼠;和糖尿病、血压正常的SD大鼠。在诱导前和每月一次监测肾功能（蛋白尿、肌酐清除率）。在体外测定诱导年龄（6-8周）和诱导后2个月和4个月大鼠的血管功能。肾血流与年龄相关，但与糖尿病或Ren 2基因无关。糖尿病大鼠和非糖尿病大鼠的肾脏重量特异性和体重特异性肾流量不同，因为糖尿病大鼠的肾脏较高，但体重较低。在血管紧张素II存在下，所有组的肾脏均显示出有效的自动调节。与SD大鼠相比，m（Ren 2）27大鼠的自主调节压力阈值更高，自主调节压力范围更广。当用罂粟碱阻断血管平滑肌活动时，压力-流量反应在组间和随时间而不同。m（Ren 2）27大鼠组在较低压力下显示出较高的肾血管阻力，表明血管硬度更大。相比之下，糖尿病SD大鼠肾脏表现出血管硬度降低。糖尿病m（Ren 2）27大鼠在4个月时血流受损，这与肌酐清除率下降相关。结果表明，在糖尿病和高血压相关的肾脏疾病中，肾滤过功能的特征性晚期下降与肾血管顺应性的变化有关。
Hill JV, Findon G, Appelhoff RJ, Endre ZH. Renal autoregulation and passive pressure-flow relationships in diabetes and hypertension. Am J Physiol Renal Physiol 299: F837-F844, 2010. First published July 21, 2010; doi:10.1152/ajprenal.00727.2009.-We investigated renal hemodynamics in isolated, perfused kidneys from rat models of diabetes and hypertension. Autoregulation and passive vascular responses were measured using stepped pressure ramps in the presence of angiotensin II (pEC50) or papaverine (0.1 mM), respectively. Male diabetic heterozygote m(Ren2)27 rats were compared with three male control groups: nondiabetic, normotensive Sprague-Dawley (SD) rats; nondiabetic, hypertensive heterozygote m(Ren2)27 rats; and diabetic, normotensive SD rats. Kidney function (proteinuria, creatinine clearance) was monitored before induction and at monthly intervals. Vascular function was measured in vitro in rats of induction age (6-8 wk) and at 2 and 4 mo postinduction. Renal flow correlated with age, but not diabetes or the Ren2 gene. Kidney weight-specific and body weight-specific renal flow differed between diabetic and nondiabetic rats because diabetic rats had higher kidney but lower body weights. Kidneys from all groups showed effective autoregulation in the presence of angiotensin II. The autoregulatory pressure threshold of m(Ren2)27 rats was higher, and the autoregulation pressure range was wider, compared with SD rats. When vascular smooth muscle activity was blocked with papaverine, pressure-flow responses differed between groups and with time. The m(Ren2) 27 rat groups showed higher renal vascular resistance at lower pressures, suggesting greater vascular stiffness. In contrast, diabetic SD rat kidneys demonstrated reduced vessel stiffness. Flow was impaired in diabetic m(Ren2) 27 rats at 4 mo, and this correlated with a decline in creatinine clearance. The results suggest that the characteristic late decline in renal filtration function in diabetes-and hypertension-related renal disease follows changes in renal vascular compliance.