Role of nitric oxide in modulating the vasoconstrictor actions of angiotensin II in preglomerular and postglomerular vessels in dogs.
Role of nitric oxide in modulating the vasoconstrictor actions of angiotensin II in preglomerular and postglomerular vessels in dogs.
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一氧化氮在调节狗肾小球前和肾小球后血管中血管紧张素 II 的血管收缩作用中的作用。
DOI：
10.1161/01.hyp.26.6.1024
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发表时间：
1995
期刊：
影响因子：
--
通讯作者：
Granger,JP
中科院分区：
文献类型：
--
作者：
Schnackenberg,CG;Wilkins,FC;Granger,JP
本研究的目的是确定一氧化氮在调节血管紧张素II（Ang II）对犬肾段阻力的血管收缩作用中的作用。为了达到这一目的，我们研究了在存在和不存在肾内一氧化氮合成抑制的情况下，肾内输注血管紧张素II对肾小球前和肾小球后阻力的影响，肾内输注NG-硝基-L-精氨酸-甲基酯，每分钟5 μg/kg。采用全肾停流技术。整个研究期间，肾动脉压伺服控制在78±2 mm Hg。肾内单独输注0.5和2.0 ng/kg/min的Ang II可增加肾血管阻力（分别为Δ0.064±0.011和Δ0.171±0.030 mm Hg/mL/min），并降低肾血流量（Δ21±4和Δ45±9 mL/min）。与这些变化相关的是，肾小球静水压力和肾小球前阻力轻微增加（分别为Δ1.1±0.9和Δ1.6±1.8 mm Hg; Δ0.008±0.005和Δ0.030±0.010 mm Hg/mL/min），肾小球后阻力显著增加（分别为Δ0.046±0.011和Δ0.116±0.026 mm Hg/mL/min）。当犬肾内输注一氧化氮合成阻断剂时，0.5和2.0 ng/kg/min的Ang II增加肾血管阻力（Δ0.271±0.058和Δ1.088±0.242 mm Hg/mL/min），减少肾血流量（Δ28±5和Δ62±9 mL/min）。然而，与赋形剂预处理形成鲜明对比的是，Ang II降低肾小球静水压力，（Δ3.4±1.5和Δ9.9±2.0 mm Hg），肾小球后阻力增加（Δ0.122±0.029和Δ0.439±0.133 mm Hg/mL/min），用一氧化氮合成抑制剂预处理的狗的肾小球前阻力增加（每分钟Δ0.109±0.031和Δ0.487±0.099 mm Hg/mL）。总之，这些数据表明，在媒介物治疗期间，停流肾中的Ang II输注对肾小球后阻力具有主要作用。然而，当一氧化氮合成被阻断时，血管紧张素II对肾小球前阻力有深远的影响。这些研究结果表明，一氧化氮可能发挥重要作用，主要是保护肾小球前血管和肾小球后血管血管在较小程度上从血管紧张素II诱导的狗肾血管收缩。
The purpose of this study was to determine the role of nitric oxide in modulating the vasoconstrictor effect of angiotensin II (Ang II) on renal segmental resistances in the dog. To achieve this objective we examined the effect of intrarenal infusions of Ang II on preglomerular and postglomerular resistances in the presence and absence of intrarenal nitric oxide synthesis inhibition established by an intrarenal infusion ofNG-nitro-l-arginine-methyl ester at 5 μg/kg per minute in dogs. The whole-kidney stop-flow technique was used. Renal artery pressure was servo-controlled at 78±2 mm Hg throughout the study. Intrarenal infusion of Ang II alone at 0.5 and 2.0 ng/kg per minute increased renal vascular resistance (Δ0.064±0.011 and Δ0.171±0.030 mm Hg/mL per minute, respectively) and decreased renal blood flow (Δ21±4 and Δ45±9 mL/min). Associated with these changes, glomerular hydrostatic pressure and preglomerular resistance increased slightly (Δ1.1±0.9 and Δ1.6±1.8 mm Hg; Δ0.008±0.005 and Δ0.030±0.010 mm Hg/mL per minute, respectively), and postglomerular resistance increased markedly (Δ0.046±0.011 and Δ0.116±0.026 mm Hg/mL per minute). When dogs were pretreated with an intrarenal infusion of the nitric oxide synthesis blocker, Ang II at 0.5 and 2.0 ng/kg per minute increased renal vascular resistance (Δ0.271±0.058 and Δ1.088±0.242 mm Hg/mL per minute) and decreased renal blood flow (Δ28±5 and Δ62±9 mL/min). However, in sharp contrast to vehicle pretreatment, Ang II decreased glomerular hydrostatic pressure (Δ3.4±1.5 and Δ9.9±2.0 mm Hg), increased postglomerular resistance (Δ0.122±0.029 and Δ0.439±0.133 mm Hg/mL per minute), and increased preglomerular resistance (Δ0.109±0.031 and Δ0.487±0.099 mm Hg/mL per minute) in dogs pretreated with the nitric oxide synthesis inhibitor. In summary, these data indicate that during vehicle treatment Ang II infusion in the stop-flow kidney had a predominant effect on postglomerular resistance. However, when nitric oxide synthesis was blocked, Ang II had a profound effect on preglomerular resistance. These findings suggest that nitric oxide may play an important role in protecting mainly preglomerular vessels and to a lesser extent postglomerular vessels from Ang II–induced renal vasoconstriction in dogs.