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首页> 外文期刊>Canadian Journal of Physiology and Pharmacology >Increased severity of renal impairment in nephritic mice lacking the EP1 receptor.
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Increased severity of renal impairment in nephritic mice lacking the EP1 receptor.

机译：缺乏EP1受体的肾病小鼠肾功能损害的严重程度增加。

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In experimental glomerulonephritis, inhibition of renal prostaglandin (PG) synthesis by nonsteroidal-anti-inflammatory drugs (NSAIDs) moderates proteinuria, yet can induce harmful effects on renal blood flow and Na+ - K+ - water balance thereby implicating 1 or more prostanoid receptor subtypes. We investigated the role of the PGE2 EP1 receptor in nephritis since it is expressed in the glomerulus, collecting duct and vasculature in which its activity might contribute to adaptive or maladaptive responses. Accordingly, a mouse model of accelerated antiglomerular basement membrane (anti-GBM) nephrotoxic serum (NTS) nephritis was induced in mice with targeted-deletion of the EP1 receptor (EP1-/-). Proteinuria was similar between wild-type (wt) and EP1-/- NTS groups, thus negating a role for this subtype in modulating the glomerular permeability barrier in this model of anti-GBM NTS. However, overall renal damage was more acute in NTS EP1-/- mice, as evidenced by the degree of glomerular mesangial matrix expansion and the frequency of tubular dilatations. These changes in renal pathology were accompanied by stronger impairment of renal function in NTS EP1-/- mice, such that levels of serum creatinine, urea, Na+, and K+ were each significantly higher than those observed in NTS wt mice. Lastly, compared with wt mice, induction of NTS more severely reduced urine osmolality and body mass in EP1-/- mice. Taken together, the increased renal impairment seen in NTS EP1-/- mice suggests that the EP1 subtype plays a compensatory role in the context of acute nephritis.
机译：在实验性肾小球肾炎中，非甾体抗炎药（NSAIDs）抑制肾前列腺素（PG）合成可减轻蛋白尿，但可能对肾血流量和Na +-K +-水平衡产生有害影响，从而牵涉一种或多种前列腺素受体亚型。我们调查了PGE2 EP1受体在肾炎中的作用，因为它在肾小球中表达，收集了导管和脉管系统，其中其活性可能有助于适应性或适应不良反应。因此，在具有靶向删除EP1受体（EP1-/-）的小鼠中诱导了小鼠加速的抗肾小球基底膜（抗GBM）肾毒性血清（NTS）肾炎模型。野生型（wt）组和EP1-/-NTS组之间的蛋白尿相似，因此在该抗GBM NTS模型中，该亚型在调节肾小球通透性屏障中的作用无效。然而，如肾小球系膜基质扩张程度和肾小管扩张频率所证实，NTS EP1-/-小鼠的整体肾脏损害更为严重。这些肾脏病理变化伴随着NTS EP1-/-小鼠肾功能的更强损伤，因此血清肌酐，尿素，Na +和K +的水平均显着高于NTS wt小鼠中观察到的水平。最后，与wt小鼠相比，NTS的诱导更加严重地降低了EP1-/-小鼠的尿渗透压和体重。两者合计，在NTS EP1-/-小鼠中观察到的肾脏损害增加表明，EP1亚型在急性肾炎的背景下起补偿作用。

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