ROLE OF EDRF (NITRIC-OXIDE) IN DIABETIC RENAL HYPERFILTRATION
ROLE OF EDRF (NITRIC-OXIDE) IN DIABETIC RENAL HYPERFILTRATION
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DOI：
10.1038/ki.1993.183
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发表时间：
1993-06-01
影响因子：
19.6
通讯作者：
AYNEDJIAN, HS
中科院分区：
文献类型：
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作者：
BANK, N;AYNEDJIAN, HS
为了研究EDRF在糖尿病高滤过中的作用，我们测定了链脲佐剂糖尿病大鼠和正常对照大鼠动脉血浆、尿液和肾静脉血中一氧化氮（NO）稳定产物NO2-/NO3-的浓度。在另外的实验中，肾脏血流动力学和血压对分级剂量的NO合成抑制剂（硝基- l -精氨酸；NLA）的反应进行了测量。我们发现STZ糖尿病大鼠（10 ~ 15天）血浆和尿液中NO2-/NO3-水平明显高于正常大鼠。在NLA输注后，糖尿病大鼠和正常大鼠的肾血流量和GFR均明显下降，尽管在所有剂量的抑制剂下，糖尿病大鼠的RBF和GFR的绝对水平仍显著升高。糖尿病大鼠的平均动脉血压（MAP）升高，但与正常大鼠相比，升高幅度明显减弱。同样，在相同剂量的NLA下，糖尿病大鼠的肾血管阻力（RVR）的增加比正常大鼠少。与正常大鼠相比，糖尿病大鼠对NLA的血管收缩反应减弱，同时尿液中NO2-/NO3-水平也有较小的降低。这些发现表明，在出现高滤过的糖尿病大鼠中，NO合成增加，这与过量的NO合成导致肾脏高滤过的观点是一致的。
In order to study the role of EDRF in diabetic hyperfiltration, the concentrations of NO2-/NO3-, the stable products of nitric oxide (NO), were measured in arterial plasma, urine, and renal venous blood in streptozotocin diabetic rats and normal control rats. In additional experiments, the renal hemodynamic and blood pressure responses to graded doses of an inhibitor of NO synthesis (Nitro-L-arginine; NLA) were measured. We found that plasma and urinary levels of NO2-/NO3- are significantly higher in STZ diabetic rats (10 to 15 days) than in normal rats. Renal blood flow and GFR fell comparably in diabetic and normal rats in response to NLA infusion, although the absolute levels of RBF and GFR remained significantly higher in the diabetic rats at all doses of the inhibitor. Mean arterial blood pressure (MAP) rose in response to NLA administration, but the increase in the diabetic rats was significantly blunted as compared with the normal rats. Similarly, renal vascular resistance (RVR) increased less in the diabetic than in the normal rats at comparable doses of NLA. The blunted vasoconstrictor responses to NLA were accompanied by a smaller reduction in the levels of NO2-/NO3- in the urine of the diabetic versus the normal rats. These findings suggest that NO synthesis is increased in diabetic rats manifesting hyperfiltration and are consistent with the view that excess NO synthesis contributes to renal hyperfiltration.