Sonnenberg H, Honrath U, Chong C K, Field L J, Veress A T
Department of Physiology, University of Toronto, ON, Canada.
Can J Physiol Pharmacol. 1994 Oct;72(10):1168-70. doi: 10.1139/y94-165.
A transgenic mouse model in which atrial natriuretic factor (ANF) expression is targeted to the liver was used to study intrarenal adjustments to the chronically elevated hormone level. Such animals, designated TTR-ANF, are characterized by reduced arterial blood pressure but similar sodium excretion compared with nontransgenic siblings. Proximal tubular micropuncture gave the following results: single-nephron filtration rate = 12.7 +/- 1.1 vs. 15.6 +/- 1.9 nL/min (TTR-ANF versus nontransgenic, ns); end-proximal tubular fluid/plasma concentration ratio of inulin = 1.93 +/- 0.09 vs. 1.97 +/- 0.15 (ns); fractional reabsorption of sodium = 45.5 +/- 2.8 vs. 46.0 +/- 3.8% (ns); fractional reabsorption of chloride = 33.6 +/- 3.3 vs. 32.4 +/- 4.1% (ns). These data indicate that life-long elevation of plasma ANF concentration was not associated with significant alteration in single-nephron filtration rate and proximal tubular function. We conclude that compensatory antinatriuretic mechanisms, localized downstream from the proximal tubule, can prevent ANF natriuresis.
一种将心房利钠因子（ANF）表达靶向肝脏的转基因小鼠模型被用于研究肾脏对长期升高的激素水平的内部调节。这种动物，称为TTR-ANF，与非转基因的同胞相比，其动脉血压降低但钠排泄相似。近端肾小管微穿刺得到以下结果：单肾单位滤过率=12.7±1.1对15.6±1.9纳升/分钟（TTR-ANF对非转基因，无显著性差异）；近端肾小管终末段液体/血浆菊粉浓度比=1.93±0.09对1.97±0.15（无显著性差异）；钠的分数重吸收=45.5±2.8对46.0±3.8%（无显著性差异）；氯的分数重吸收=33.6±3.3对32.4±4.1%（无显著性差异）。这些数据表明，血浆ANF浓度的终生升高与单肾单位滤过率和近端肾小管功能的显著改变无关。我们得出结论，位于近端肾小管下游的代偿性抗利钠机制可以防止ANF利钠作用。
