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低剂量血管紧张素II输注对髓袢节段重吸收的影响:大鼠自由流微穿刺研究

Effects of low-dose angiotensin II infusion on loop segment reabsorption: a free-flow micropuncture study in rats.

作者信息

Fransen R, Boer W H, De Roos R, Boer P, Koomans H A

机构信息

Department of Nephrology and Hypertension, University Hospital Utrecht, The Netherlands.

出版信息

Clin Sci (Lond). 1995 Mar;88(3):351-8. doi: 10.1042/cs0880351.

DOI:10.1042/cs0880351
PMID:7736706
Abstract
  1. Little direct information is available on the actions of angiotensin II beyond the proximal tubule. We therefore studied the effect of a mildly vasoconstrictive dose of angiotensin II on tubular handling of water, sodium (Na+) and lithium (Li+) in rats by means of free-flow micropuncture at the late proximal tubule and the early distal tubule. 2. Endogenous angiotensin II was suppressed by pretreatment with enalapril. Compared with a control group, angiotensin II increased mean arterial pressure by 15 mmHg. Glomerular filtration rate decreased from 1.32 +/- 0.05 to 1.10 +/- 0.05 ml/min, Na+ excretion from 0.43 +/- 0.09 to 0.13 +/- 0.03 mumol/min, fractional delivery of water at the late proximal tubule from 50.1 +/- 1.7 to 42.9 +/- 3.2%, fractional delivery of Na+ at the late proximal tubule from 46.5 +/- 1.3 to 39.1 +/- 3.5% and fractional delivery of water at the early distal tubule from 26.4 +/- 1.4 to 21.9 +/- 1.0% (P < 0.05 for each variable). Fractional delivery of Na+ at the early distal tubule did not change significantly. 3. Similar experiments were performed during partial aortic constriction to exclude the effects of increased perfusion pressure. The data obtained were similar, except that in this group the fractional delivery of Na+ at the early distal tubule decreased from 8.6 +/- 0.7 to 6.8 +/- 0.9% (P < 0.05). 4. The relation between late proximal tubule Na+ delivery and Na+ reabsorption between late proximal and early distal tubule was not disturbed by angiotensin II. For water, however, this relation tended to shift to a higher reabsorption rate.(ABSTRACT TRUNCATED AT 250 WORDS)
摘要
  1. 关于血管紧张素II在近端小管之外的作用,几乎没有直接信息。因此,我们通过对大鼠近端小管晚期和远端小管早期进行自由流微量穿刺,研究了轻度血管收缩剂量的血管紧张素II对肾小管水、钠(Na+)和锂(Li+)处理的影响。2. 用依那普利预处理可抑制内源性血管紧张素II。与对照组相比,血管紧张素II使平均动脉压升高15 mmHg。肾小球滤过率从1.32±0.05降至1.10±0.05 ml/分钟,Na+排泄量从0.43±0.09降至0.13±0.03 μmol/分钟,近端小管晚期水的分数输送率从50.1±1.7降至42.9±3.2%,近端小管晚期Na+的分数输送率从46.5±1.3降至39.1±3.5%,远端小管早期水的分数输送率从26.4±1.4降至21.9±1.0%(每个变量P<0.05)。远端小管早期Na+的分数输送率无显著变化。3. 在部分主动脉缩窄期间进行了类似实验,以排除灌注压升高的影响。获得的数据相似,只是在该组中,远端小管早期Na+的分数输送率从8.6±0.7降至6.8±0.9%(P<0.05)。4. 血管紧张素II并未干扰近端小管晚期Na+输送与近端小管晚期和远端小管早期之间Na+重吸收的关系。然而,对于水而言,这种关系倾向于向更高的重吸收率转变。(摘要截断于250字)

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