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首页> 外文期刊>Life sciences >Blunted renal dopaminergic system activity in HgCl2-induced membranous nephropathy.
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Blunted renal dopaminergic system activity in HgCl2-induced membranous nephropathy.

机译：HgCl2引起的膜性肾病的肾脏多巴胺能系统活动减弱。

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The present study evaluated the possible role of the renal dopaminergic system in the sodium retention of HgCl2-induced nephrotic syndrome. The time courses of urinary excretion of sodium, protein, dopamine and the precursor l-3,4-dihydroxyphenylalanine (L-Dopa) were evaluated in HgCl2-treated and control rats up to day 21. The renal aromatic l-amino acid decarboxylase (AADC) activity, the enzyme responsible for the synthesis of renal dopamine, was evaluated during negligible proteinuria accompanied with enhanced sodium retention (day 7), increased proteinuria accompanied with greatest sodium retention (day 14) as well as during increased proteinuria accompanied with negative sodium balance (day 21). Also, the influence of volume expansion (VE, 5% bw) and the effects of the D1-like agonist fenoldopam (10 microg kg bw(-1) min(-1)) on natriuresis and on proximal tubular Na+,K+-ATPase activity were examined on day 14. The daily urinary dopamine output and urinary dopamine/L-Dopa ratios were reduced in HgCl2-treated rats from day 2 and beyond. This was accompanied by a marked decrease in renal AADC throughout the study. During VE, the fenoldopam-induced inhibition of proximal tubular Na+,K+-ATPase activity was similar between HgCl2-treated and control rats. However, the urinary sodium excretion during fenoldopam infusion was markedly increased by 60% to 120% in control rats but was not altered in HgCl2-treated rats. It is concluded that HgCl2 nephrosis is associated with a blunted renal dopaminergic system activity. However, the lack of renal dopamine in HgCl2 nephrosis does not appear to be related with the overall renal sodium retention in a state of proteinuria.
机译：本研究评估了肾脏多巴胺能系统在HgCl2引起的肾病综合征的钠retention留中的可能作用。在经过HgCl2处理的大鼠和对照组中，评估了尿排泄钠，蛋白质，多巴胺和前体1，3，4-二羟基苯丙氨酸（L-Dopa）的时程，直至第21天。肾芳香族l-氨基酸脱羧酶（在可忽略不计的蛋白尿伴有钠保留增加的情况下（第7天），蛋白尿增加与钠保留量最大的情况下（第14天）以及蛋白尿增加并伴有负钠的过程中，评估了AADC）活性（负责肾脏多巴胺合成的酶）余额（第21天）。同样，体积膨胀的影响（VE，5％bw）和D1样激动剂非诺多m（10 microg kg bw（-1）min（-1））对利尿和近端肾小管Na +，K + -ATPase的影响在第14天检查活性。从HgCl 2处理的大鼠开始，从第2天开始以及以后，尿中多巴胺的每日输出量和尿中多巴胺/ L-Dopa之比降低。在整个研究过程中，伴有肾脏AADC的显着下降。在VE期间，用HgCl2处理的大鼠和对照大鼠中非诺多巴诱导的对近端小管Na +，K + -ATPase活性的抑制作用相似。然而，在对照组大鼠中，非诺多m输注过程中尿钠排泄显着增加了60％至120％，但在用HgCl2处理的大鼠中并未改变。结论是HgCl2肾病与肾脏多巴胺能系统活动减弱有关。但是，HgCl2肾病中缺乏肾多巴胺似乎与蛋白尿状态的总体肾钠retention留没有关系。

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