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Effects of losartan, in monotherapy or in association with hydrochlorothiazide, in chronic nephropathy resulting from losartan treatment during lactation

机译：氯沙坦，单药治疗或与氢氯噻嗪联合治疗对哺乳期氯沙坦治疗引起的慢性肾病的影响

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Fanelli C, Fernandes BH, Machado FG, Okabe C, Malheiros DM, Fujihara CK, Zatz R. Effects of losartan, in monotherapy or in association with hydrochlorothiazide, in chronic nephropathy resulting from losartan treatment during lactation. Am J Physiol Renal Physiol 301: F580-F587, 2011. First published June 8, 2011; doi:10.1152/ajprenal.00042.2011.-We recently standardized a model (L(Lact)) of severe chronic kidney disease based on impaired nephrogenesis by suppression of angiotensin II activity during lactation (Machado FG, Poppi EP, Fanelli C, Malheiros DM, Zatz R, Fujihara CK. Am J Physiol Renal Physiol 294: F1345-F1353, 2008). In this new study of the L(Lact) model, we sought to gain further insight into renal injury mechanisms associated with this model and to verify whether the renoprotection obtained with the association of the angiotensin II receptor blocker losartan (L) and hydrochlorothiazide (H), which arrested renal injury in the remnant kidney model, would provide similar renoprotection. Twenty Munich-Wistar dams, each nursing six pups, were divided into control, untreated, and L(Lact) groups, given losartan (L; 250 mg.kg(-1).day(-1)) until weaning. The male LLact offspring remained untreated until 7 mo of age, when renal functional and structural parameters were studied in 17 of them, used as pretreatment control (L(Lact)Pre), and followed no further. The remaining rats were then divided among groups L(Lact) + V, untreated; L(Lact) + L, given L (50 mg.kg(-1).day(-1)) now as a therapy; L(Lact) + H, given H (6 mg.kg(-1).day(-1)); and L(Lact) + LH, given L and H. All parameters were reassessed 3 mo later in these groups and in age-matched controls. At this time, L(Lact) rats exhibited hypertension, severe albuminuria, glomerular damage, marked interstitial expansion/inflammation, enhanced cell proliferation, myofibroblast infiltration, and creatinine retention. L monotherapy normalized albuminuria and prevented hypertension and the progression of renal injury, inflammation, and myofibroblast infiltration. In contrast to the remnant model, the LH combination promoted only slight additional renoprotection, perhaps because of a limited tendency to retain sodium in L(Lact) rats.
机译：Fanelli C，Fernandes BH，Machado FG，Okabe C，Malheiros DM，Fujihara CK，Zatz R.氯沙坦在单一疗法中或与氢氯噻嗪联用对泌乳期间氯沙坦治疗导致的慢性肾病的影响。 Am J Physiol Renal Physiol 301：F580-F587，2011年。2011年6月8日首次发布； doi：10.1152 / ajprenal.00042.2011.-我们最近通过抑制泌乳过程中血管紧张素II的活性（Machado FG，Poppi EP，Fanelli C，Malheiros DM， Zatz R，Fujihara CK.Am J Physiol Renal Physiol 294：F1345-F1353，2008）。在L（Lact）模型的这项新研究中，我们试图获得与该模型相关的肾脏损伤机制的进一步见解，并验证是否通过血管紧张素II受体阻滞剂氯沙坦（L）和氢氯噻嗪（H ）（可在残余肾脏模型中阻止肾脏损伤）将提供类似的肾脏保护作用。二十只慕尼黑-维斯塔水坝，每只饲养六只幼崽，分为对照组，未处理组和L（Lact）组，给予氯沙坦（L; 250 mg.kg（-1）.day（-1））直至断奶。雄性LLact后代直到7个月大时仍未得到治疗，当时在其中的17个中研究了肾功能和结构参数，将其用作治疗前对照（L（Lact）Pre），之后不再进行治疗。然后将剩余的大鼠分为未经处理的L（Lact）+ V组。 L（Lact）+ L，现在给予L（50 mg.kg（-1）.day（-1））作为治疗； L（乳酸）+ H，给予H（6 mg.kg（-1）.day（-1））;和L（Lact）+ LH，分别为L和H。在这些组和年龄匹配的对照组中，所有参数均在3个月后重新评估。此时，L（Lact）大鼠表现出高血压，严重的白蛋白尿，肾小球损害，明显的间质扩张/炎症，增强的细胞增殖，成肌纤维细胞浸润和肌酐保留。 L单药治疗可使白蛋白尿正常化，并预防高血压以及肾损伤，炎症和成纤维细胞浸润的发展。与残余模型相反，LH组合仅促进了轻微的额外肾脏保护作用，这可能是由于在L（Lact）大鼠中保留钠的趋势有限。

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