Reduced sensitivity of the renal circulation to angiotensin II in pregnant rats.
Reduced sensitivity of the renal circulation to angiotensin II in pregnant rats.
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妊娠大鼠肾循环对血管紧张素 II 的敏感性降低。
DOI：
10.1161/01.hyp.30.3.580
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发表时间：
1997
期刊：
影响因子：
--
通讯作者：
Granger,JP
中科院分区：
文献类型：
--
作者：
Novak,J;Reckelhoff,J;Bumgarner,L;Cockrell,K;Kassab,S;Granger,JP
妊娠期和妊娠高血压综合征患者的肾循环发生显著变化。虽然许多研究表明，升压反应血管紧张素II（Ang II）是减少在怀孕期间，目前尚不清楚是否这种改变的敏感性血管紧张素II发生在肾循环。本研究的第一个目的是确定是否在中期妊娠大鼠的肾血管反应性外源性血管紧张素II的改变。所有大鼠静脉注射转化酶抑制剂卡托普利（20 μg · kg-1· min-1）以阻断内源性Ang II的形成。对照期后，通过肾上主动脉导管将Ang II以10 ng · kg-1· min-1的剂量注入肾动脉50 min。在麻醉的未孕大鼠中，Ang II使肾血浆流量（RPF）降低39%（5.0±0.4至3.1±0.4 mL/min），肾小球滤过率（GFR）降低39%（1.9±0.1至1.16±0.2 mL/min），尿流量降低47%（22.1±5.6至12.3±4.8 μL/min）。相比之下，Ang II对麻醉孕鼠的RPF、GFR和尿流量无明显影响。 由于一氧化氮（NO）先前已报道，以调节肾血管的行动，血管紧张素II在正常动物和NO的合成被认为是在怀孕期间升高，本研究探讨了NO的作用，在衰减肾血管紧张素II的反应。L-NAME预处理组孕鼠的动脉压高于对照组，RPF低于对照组。然而，在L-NAME预处理的妊娠大鼠肾脏对Ang II的反应与对照妊娠大鼠相似。这些数据表明，肾循环在怀孕期间对Ang II的敏感性降低。我们还发现，NO合成抑制不改变麻醉孕鼠肾对Ang Ⅱ的反应减弱。
The renal circulation undergoes significant changes during pregnancy and pregnancy-induced hypertension. Although numerous studies indicate that the pressor response to angiotensin II (Ang II) is reduced during pregnancy, it is unclear as to whether this altered sensitivity to Ang II occurs in the renal circulation. The first aim of this study was to determine whether the renal vascular responsiveness to exogenous Ang II is altered in the midterm pregnant rat. All rats were pretreated with an intravenous infusion of the converting-enzyme inhibitor captopril (20 μg · kg−1· min−1) to block endogenous Ang II formation. Following a control period, Ang II was infused at a dose of 10 ng · kg−1· min−1for 50 minutes into the renal arteries via a suprarenal aortic catheter. In anesthetized virgin rats, Ang II markedly decreased renal plasma flow (RPF) by 39% (5.0±0.4 to 3.1±0.4 mL/min), glomerular filtration rate (GFR) by 39% (1.9±0.1 to 1.16±0.2 mL/min), and urine flow by 47% (22.1±5.6 to 12.3±4.8 μL/min). In contrast, Ang II had no significant effect on RPF, GFR, and urine flow in the anesthetized pregnant rats. Since nitric oxide (NO) has been previously reported to modulate the renal vascular actions of Ang II in normal animals and NO synthesis is thought to be elevated in pregnancy, this study examined the role of NO in the attenuated renal response to Ang II. In pregnant rats pretreated with L-NAME, the arterial pressure was higher and RPF was lower than in the control pregnant rats. However, the renal response to Ang II in the L-NAME–pretreated pregnant rats was similar to control pregnant rats. These data indicate that the renal circulation has a reduced sensitivity to Ang II during pregnancy. We also found that NO synthesis inhibition does not alter the attenuated renal response to Ang II in the anesthetized pregnant rats.