Impaired renal hemodynamic response to protein feeding in dogs with experimental Fanconi syndrome.
Impaired renal hemodynamic response to protein feeding in dogs with experimental Fanconi syndrome.
复制标题
患有实验性范可尼综合征的狗对蛋白质喂养的肾血流动力学反应受损。
DOI：
10.1152/ajprenal.1991.261.1.f14
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发表时间：
1991
期刊：
影响因子：
--
通讯作者：
Young,EW
中科院分区：
文献类型：
--
作者：
Woods,LL;Young,EW
这些研究旨在检验蛋白质刺激的肾血管舒张需要完整的近端肾小管功能这一假设。在正常的慢性仪器清醒的狗，一餐生牛肉（10 g/kg）引起肾小球滤过率（GFR）显着增加，从63 +/- 5至94 +/- 10 ml/min后90分钟，而血浆α-氨基氮从3.9 +/- 0.2上升到6.7 +/- 0.6 mg/dl。在另一组狗中，用马来酸（25 mg/kg iv，pH 7.3）诱导实验性范可尼综合征（全身性近端肾小管功能障碍）。给予马来酸后，GFR从91 +/- 18降至66 +/- 9 ml/min，而Na+排泄从24 +/- 8升至176 +/- 24 mu eq/min，α-氨基氮排泄从82 +/- 40升至148 +/- 47 μ g/min，葡萄糖排泄从0.2 +/- 0.1上升到6.1 +/- 1.0 mg/min。作为对随后的肉食的反应，血浆α-氨基氮从3.8 +/- 0.4显著上升到6.2 +/- 0.5 mg/dl，但GFR没有变化，在接下来的120分钟内平均66 +/- 9 ml/min。这些结果表明，正常的近端肾小管功能是蛋白质刺激的肾血管舒张发生所必需的。这一发现是一致的假设，肾小管肾小球反馈机制可能参与介导的正常肾脏血液动力学反应的蛋白质喂养。
These studies were designed to test the hypothesis that intact proximal tubular function is required for protein-stimulated renal vasodilation. In normal chronically instrumented conscious dogs, a meal of raw beef (10 g/kg) caused glomerular filtration rate (GFR) to increase significantly from 63 +/- 5 to 94 +/- 10 ml/min after 90 min, while plasma alpha-amino nitrogen rose from 3.9 +/- 0.2 to 6.7 +/- 0.6 mg/dl. In another group of dogs experimental Fanconi syndrome (generalized proximal tubular dysfunction) was induced with maleic acid (25 mg/kg iv, pH 7.3). GFR fell slightly but significantly from 91 +/- 18 to 66 +/- 9 ml/min after maleic acid, while Na+ excretion rose from 24 +/- 8 to 176 +/- 24 mu eq/min, alpha-amino nitrogen excretion rose from 82 +/- 40 to 148 +/- 47 micrograms/min, and glucose excretion rose from 0.2 +/- 0.1 to 6.1 +/- 1.0 mg/min. In response to a subsequent meat meal, plasma alpha-amino nitrogen rose significantly from 3.8 +/- 0.4 to 6.2 +/- 0.5 mg/dl, but GFR did not change, averaging 66 +/- 9 ml/min over the next 120 min. These results suggest that normal proximal tubular function is necessary for protein-stimulated renal vasodilation to occur. This finding is consistent with the hypothesis that the tubuloglomerular feedback mechanism may be involved in mediating the normal renal hemodynamic response to protein feeding.