Renal function in mice: effects of volume expansion and angiotensin II.

Renal function in mice: effects of volume expansion and angiotensin II.
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发表时间:
1999-12
期刊:
Journal of the American Society of Nephrology : JASN
影响因子:
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通讯作者:
L. C̆ervenka;Kenneth D. Mitchell;L. Navar
L. C̆ervenka;Kenneth D. Mitchell;L. Navar
中科院分区:
其他
文献类型:
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作者:
L. C̆ervenka;Kenneth D. Mitchell;L. Navar

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本研究旨在验证一种评估麻醉小鼠肾功能的简单方法,并研究急性扩容对肾脏血流动力学的反应,以及血管紧张素II(AngII)同时输注对这些反应的影响。用菊粉清除法和对氨基马尿酸清除法测定了三组雄性C57BL/6小鼠的肾小球滤过率(GFR)和肾血浆流量(RPF)。为了避免与重复采血相关的低血压,在三次定时尿液采集后采集了一次血样。测定肾功能和平均动脉压(MAP),分别在等容状态(2.5微l/min,静注,n=7)、等渗盐水扩容(12.5微l/min,静注,n=5)和扩容合并血管紧张素转换酶抑制剂(AngII,5 ng/min,x g,n=5)。对照组MAP为77+/-2 mm Hg,单纯扩容对MAP无显著影响(83+/-2 mm Hg),但导致GFR和RPF均显著升高(分别为1.35+/-0.14vs1.01+/-0.1ml/minxg和11.26+/-1.39vs6.29+/-0.5ml/ming)。扩容时应用血管紧张素转换酶抑制剂使MAP显著升高(100+/-3 mm Hg,P<0.05),并抑制扩容引起的GFR和RPF升高(分别为0.77+/-0.08和5.35+/-0.48ml/min×g)。容量扩张还导致绝对和部分钠排泄显著增加(分别为6.1+/-1.0vs0.62+/-0.2microEq/minxg和3.1+/-0.7vs0.4+/-0.1%)。血管紧张素转换酶抑制剂可减弱绝对钠排泄反应和部分钠排泄反应(分别为3.4+/-1.2微Eq/min×g和2.5+/-0.5%)。目前的研究结果表明,麻醉小鼠对等渗盐水体积扩张有明显的肾脏血流动力学和排泄反应。同时输注血管紧张素转换酶抑制了这些反应,尽管动脉压有更大的升高。
The present study was performed to validate a simple means for assessing renal function in anesthetized mice and to characterize the renal hemodynamic responses to acute volume expansion and how these responses are altered by concurrent angiotensin II (AngII) infusions. Inulin and para-aminohippurate clearances were used to assess GFR and renal plasma flow (RPF) in three groups of male C57Bl/6 mice anesthetized with inactin (100 mg/kg, intraperitoneally) and ketamine (10 mg/kg). To avoid the hypotension associated with repeated blood sampling, a single blood sample was taken after three timed urine collections. Renal function and mean arterial pressure (MAP) were measured under euvolemic conditions (2.5 microl/min, intravenously, n = 7) during isotonic saline volume expansion (12.5 microl/min, intravenously, n = 5) and during volume expansion with concurrent AngII infusion (5 ng/min x g, n = 5). MAP in the control group was 77 +/- 2 mmHg; volume expansion alone did not change MAP significantly (83 +/- 2 mmHg), but led to significantly greater values in both GFR and RPF (1.35 +/- 0.14 versus 1.01 +/- 0.1 ml/min x g and 11.26 +/- 1.39 versus 6.29 +/- 0.5 ml/min x g, respectively). Infusion of AngII during volume expansion led to significant elevations of MAP (100 +/- 3 mmHg, P < 0.05) and prevented the increases in GFR and RPF elicited by volume expansion (0.77 +/- 0.08 and 5.35 +/- 0.48 ml/min x g, respectively). Volume expansion also elicited marked increases in absolute and fractional sodium excretion (6.1 +/- 1.0 versus 0.62 +/- 0.2 microEq/min x g and 3.1 +/- 0.7 versus 0.4 +/- 0.1%, respectively). AngII infusion attenuated the absolute and fractional sodium excretion responses to volume expansion (3.4 +/- 1.2 microEq/min x g and 2.5 +/- 0.5%, respectively). The present findings demonstrate that anesthetized mice exhibit marked renal hemodynamic and excretory responses to isotonic saline volume expansion. Concomitant AngII infusion attenuates these responses in spite of greater increases in arterial pressure.