Continuously measured renal blood flow does not increase in diabetes if nitric oxide synthesis is blocked.
Continuously measured renal blood flow does not increase in diabetes if nitric oxide synthesis is blocked.
复制标题
如果一氧化氮合成受阻，连续测量的糖尿病肾血流量不会增加。
DOI：
10.1152/ajprenal.00004.2008
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发表时间：
2008
期刊：
影响因子：
--
通讯作者：
Brands,MichaelW
中科院分区：
文献类型：
--
作者：
Bell,TracyD;DiBona,GeraldF;Biemiller,Rachel;Brands,MichaelW
This study used 16 h/day measurement of renal blood flow (RBF) and arterial pressure (AP) to determine the role of nitric oxide (NO) in mediating the renal vasodilation caused by onset of type 1 diabetes. The AP and RBF power spectra were used to determine the autoregulatory efficiency of the renal vasculature. Rats were instrumented with artery and vein catheters and a Transonic flow probe on the left renal artery and were divided randomly into four groups: control (C), diabetes (D), control plus nitro-l-arginine methyl ester (l-NAME; CL), and diabetes plusl-NAME (DL). Mean AP averaged 90 ± 1 and 121 ± 1 mmHg in the D and DL groups, respectively, during the control period, and RBF averaged 5.9 ± 1.2 and 5.7 ± 0.7 ml/min, respectively. Respective C and CL groups were not different. Onset of diabetes (streptozotocin 40 mg/kg iv) in D rats increased RBF gradually, but it averaged 55% above control byday 14. In DL rats, on the other hand, RBF remained essentially constant, tracking with RBF in the nondiabetic C and CL groups for the 2-wk period. Diabetes did not change mean AP in any group. Transfer function analysis revealed impaired dynamic autoregulation of RBF overall, including the frequency range of tubuloglomerular feedback (TGF), andl-NAME completely prevented those changes as well. These data strongly support a role for NO in causing renal vasodilation in diabetes and suggest that an effect of NO to blunt RBF autoregulation may play an important role.
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糖尿病大鼠肾一氧化氮对超滤作用的分析。
DOI：
10.1067/mlc.2001.112691
发表时间：
2001
期刊：
The Journal of laboratory and clinical medicine.
影响因子：
--
作者：
Schwartz,D;Schwartz,IF;Blantz,RC
通讯作者：
Blantz,RC
腺苷诱导糖尿病大鼠肾血管收缩：一氧化氮的作用。
DOI：
10.1152/ajprenal.1999.276.3.f340
发表时间：
1999
期刊：
The American journal of physiology
影响因子：
--
作者：
Pflueger,AC;Osswald,H;Knox,FG
通讯作者：
Knox,FG
致密斑衍生的一氧化氮调节肾小球毛细血管压力。
影响因子：
19.6
作者：
C. Thorup;A. Erik;G. Persson
通讯作者：
G. Persson
糖尿病发作时通过血管紧张素 II 和一氧化氮控制动脉压。
影响因子：
3.2
作者：
Brands,MichaelW;Cloud,LeslieJ
通讯作者：
Cloud,LeslieJ
影响因子：
19.6
作者：
Keynan, S;Hirshberg, B;Raz, I
通讯作者：
Raz, I