Regional blood flow responses to acute ANG II infusion: effects of nitric oxide synthase inhibition.
Regional blood flow responses to acute ANG II infusion: effects of nitric oxide synthase inhibition.
复制标题
对急性 ANG II 输注的局部血流反应：一氧化氮合酶抑制的影响。
DOI：
10.1097/00005344-199907000-00019
复制
发表时间：
1999
影响因子：
3
通讯作者：
Stebbins,CL
中科院分区：
文献类型：
--
作者：
Symons,JD;Musch,TI;Hageman,KS;Stebbins,CL
我们假设一氧化氮（NO）对抗清醒大鼠急性血管紧张素II（ANG II）输注引起的局部血管收缩。在不存在和存在NO合酶（NOS）抑制[N-硝基-L-精氨酸甲酯（L-NAME），0.25或1 mg/kg，ia]的情况下，在ANG II输注（0.05或1 μg/kg/min，ia）之前和2 min时测量和/或计算平均动脉压（MAP）、血流量和血管传导性（局部血流量/MAP; ml/min/100 g/mm Hg）。ANG II仅在NOS抑制后才降低胃和后肢电导。例如，虽然0.05 μg/kg/min ANG II不会减弱胃内传导（即，1.04±0.08至0.93±0.12 ml/min/100 g/mm Hg），但当在0.25 mg/kg L-NAME后输注ANG II时，该变量降低（即，0.57±0.14至0.34±0.05 ml/min/100 g/mm Hg; p< 0.05）。此外，尽管给予1 μg/kg/min ANG II前后后肢电导相似（即，分别为0.13±0.01和0.09±0.02），但当在1 mg/kg L-NAME后输注ANG II时，该变量降低（即，分别为0.07±0.01和0.02±0.00; p< 0.05）。这些发现表明，NO反对血管紧张素II诱导的血管收缩在胃和后肢。相反，无论是否存在NOS抑制，两种剂量的ANG II均降低（p< 0.05）肾脏和小肠及大肠的血管传导性，而L-NAME后绝对血管传导性较低（p< 0.05）。例如，1 μg/kg ANG II使肾电导从3.34±0.31降低至1.22±0.14（p< 0.05）。1 mg/kg L-NAME后，ANG II给药期间肾电导从1.39±0.18降至0.72±0.16（p< 0.05）。因此，NOS抑制和ANG II的收缩作用在这些循环中是相加的。两者合计，我们的研究结果表明，NO的能力，反对血管紧张素II引起的收缩是不均匀的区域环流。
We hypothesized that nitric oxide (NO) opposes regional vasoconstriction caused by acute angiotensin II (ANG II) infusion in conscious rats. Mean arterial pressure (MAP), blood flow, and vascular conductance (regional blood flow/MAP; ml/min/100 g/mm Hg) were measured and/or calculated before and at 2 min of ANG II infusion (0.05 or 1 μg/kg/min, ia) in the absence and presence of NO synthase (NOS) inhibition [N G-nitro-L-arginine methyl ester (L-NAME), 0.25 or 1 mg/kg, ia]. ANG II reduced stomach and hindlimb conductance only after NOS inhibition. For example, whereas 0.05 μg/kg/min ANG II did not attenuate conductance in the stomach (ie, 1.04±0.08 to 0.93±0.12 ml/min/100 g/mm Hg), this variable was reduced (ie, 0.57±0.14 to 0.34±0.05 ml/min/100 g/mm Hg; p< 0.05) when ANG II was infused after 0.25 mg/kg L-NAME. In addition, whereas hindlimb conductance was similar before and after administering 1 μg/kg/min ANG II (ie, 0.13±0.01 and 0.09±0.02, respectively), this variable was reduced (ie, 0.07±0.01 and 0.02±0.00, respectively; p< 0.05) when ANG II was infused after 1 mg/kg L-NAME. These findings indicate that NO opposes ANG II-induced vasoconstriction in the stomach and hindlimb. In contrast, whereas both doses of ANG II decreased (p< 0.05) vascular conductance in the kidneys and small and large intestine regardless of whether NOS inhibition was present, absolute vascular conductance was lower (p< 0.05) after L-NAME. For example, 1 μg/kg ANG II reduced renal conductance from 3.34±0.31 to 1.22±0.14 (p< 0.05). After 1 mg/kg L-NAME, renal conductance decreased from 1.39±0.18 to 0.72±0.16 (p< 0.05) during ANG II administration. Therefore the constrictor effects of NOS inhibition and ANG II are additive in these circulations. Taken together, our results indicate that the ability of NO to oppose ANG II-induced constriction is not homogeneous among regional circulations.