Matsumura Y, Egi Y, Maekawa H, Miura A, Murata S, Morimoto S
Department of Pharmacology, Osaka University of Pharmaceutical Sciences, Japan.
Biol Pharm Bull. 1995 Apr;18(4):496-500. doi: 10.1248/bpb.18.496.
We investigated whether endogenous nitric oxide (NO) has a role as an inhibitory modulator of norepinephrine (NE)- and angiotensin II (Ang II)-induced renal effects in anesthetized dogs. Intrarenal arterial infusion of NE (100 ng/kg/min) or Ang II (10 ng/kg/min) decreased renal blood flow (RBF), glomerular filtration rate (GFR) and urine formation. The NE- or Ang II-induced renal effects were augmented by the intrarenal administration of a NO synthase inhibitor, NG-nitro-L-arginine (NOARG), at doses (10 and 40 micrograms/kg/min) which did not affect the mean arterial blood pressure and heart rate. The stimulating activity of NOARG on NE- or Ang II-induced renal effects were abolished by the simultaneous administration of L-arginine, a NO precursor. These findings suggest that endogenous NO, which is probably generated within the kidney, functions as an inhibitory modulator in NE- or Ang II-induced renal vasoconstriction and antidiuresis.
我们研究了内源性一氧化氮（NO）在麻醉犬中是否作为去甲肾上腺素（NE）和血管紧张素II（Ang II）诱导的肾脏效应的抑制性调节剂发挥作用。肾内动脉输注NE（100 ng/kg/min）或Ang II（10 ng/kg/min）可降低肾血流量（RBF）、肾小球滤过率（GFR）和尿液生成。在不影响平均动脉血压和心率的剂量（10和40微克/千克/分钟）下，肾内给予一氧化氮合酶抑制剂NG-硝基-L-精氨酸（NOARG）可增强NE或Ang II诱导的肾脏效应。同时给予L-精氨酸（一种NO前体）可消除NOARG对NE或Ang II诱导的肾脏效应的刺激活性。这些发现表明，可能在肾脏内产生的内源性NO在NE或Ang II诱导的肾血管收缩和抗利尿中起抑制性调节剂的作用。
