Low concentrations of ANP cause pressure-dependent natriuresis in the isolated kidney.
Low concentrations of ANP cause pressure-dependent natriuresis in the isolated kidney.
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低浓度的 ANP 会在离体肾脏中引起压力依赖性尿钠排泄。
DOI：
10.1152/ajprenal.1988.255.3.f391
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发表时间：
1988
期刊：
影响因子：
--
通讯作者：
J. Ledingham
中科院分区：
文献类型：
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作者：
J. Firth;A. Raine;J. Ledingham
肾灌注压的改变对离体灌注大鼠肾对病理生理范围内的α-人心钠素（ANP）浓度的反应的影响已被检查。在90 mmHg灌注压下，50、200和1，000 pmol/l的ANP浓度对任何检测参数均无影响。在灌注压为130 mmHg时，50 pmol/l ANP使钠排泄（UNa V）增加3.13 +/- 0.68 mumol/min，而对照组下降0.33 +/- 1.04 mumol/min（P <0.02）;钠排泄分数（FENa）升高1.45 +/- 0.36% vs. -0.12 +/- 0.47%（P <0.05）;肾小球滤过率（GFR）不变。在200和1，000 pmol/l时，观察到UNa V和FENa的较大变化;仅在1，000 pmol/l时观察到对GFR的显著影响。相比之下，速尿（呋塞米）在浓度为10和100 μ mol/L是利钠在90和130毫米汞柱，较小的绝对，但更大的比例变化被视为在较低的压力。结论：1）离体肾脏对ANP的反应严重依赖于灌注压，2）在升高的灌注压水平下，离体肾脏可以对生理和病理生理范围内的ANP水平作出反应。
The effect of alteration in renal perfusion pressure on the response of the isolated perfused rat kidney to concentrations of alpha-human atrial natriuretic peptide (ANP) within the pathophysiological range has been examined. At a perfusion pressure of 90 mmHg ANP concentrations of 50, 200, and 1,000 pmol/l were without effect on any parameter tested. At a perfusion pressure of 130 mmHg 50 pmol/l ANP produced an increase of 3.13 +/- 0.68 mumol/min in sodium excretion (UNa V), compared with a fall of 0.33 +/- 1.04 mumol/min in controls (P less than 0.02); fractional excretion of sodium (FENa) rose by 1.45 +/- 0.36% vs. -0.12 +/- 0.47% (P less than 0.05); glomerular filtration rate (GFR) was unchanged. At 200 and 1,000 pmol/l larger changes in UNa V and FENa were seen; only at 1,000 pmol/l was a significant effect on GFR observed. In contrast, frusemide (furosemide) at concentrations of 10 and 100 mumol/l was natriuretic at both 90 and 130 mmHg, with lesser absolute but greater proportional changes being seen at the lower pressure. It was concluded 1) the response of the isolated kidney to ANP is critically dependent on perfusion pressure, 2) at elevated levels of perfusion pressure the isolated kidney can respond to levels of ANP within the upper physiological and pathophysiological range.