肾素-血管紧张醛固酮系统潜在药物阻断的实验性糖尿病发展动态中大鼠离子调节肾功能的特点

О. Olenovych
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On the 11th day of EDM, thesodium filtration charge increased with the development of hyponatremia, proximal anddistal sodium reabsorption standardized in volume of glomerular filtrate (GF) decreased,kaliuresis was suppressed, and sodium-free water clearance elevated. In case of 26-daylong EDM, the sodium filtration charge decreased, its absolute and relative reabsorption,the distal sodium reabsorption standardized by GF increased. Kaliuresis increased. In46-day long EDM, the sodium filtration charge decreased, and hyponatremia enhanced.Absolute and relative sodium reabsorption reduced due to both – proximal and distal.Kaliuresis augmented, the clearance of sodium-free water declined.Conclusions. 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引用次数: 0

摘要

本研究旨在探讨肾素-血管紧张素-醛固酮系统(RAAS)在四氧嘧啶诱导的实验性糖尿病(EDM)中离子调节性肾功能紊乱中的作用。材料和方法。实验以78只白色非线性雄性大鼠为实验对象,这些大鼠有11、26和46天的四氧嘧啶诱导的EDM,并通过给予卡托普利对RAAS进行潜在的药物阻断。用清除率法研究了水2小时利尿条件下肾脏的调节功能。四氧嘧啶诱导的EDM大鼠RAAS的药物阻断导致实验各阶段尿钠加剧:尿钠离子浓度、其排泄和清除增加。EDM第11天,随着低钠血症的发展,钠滤过电荷增加,近端和远端钠重吸收标准化肾小球滤液(GF)体积减少,钾尿抑制,无钠水清除率升高。EDM 26 d时,钠的过滤电荷减少,其绝对和相对重吸收量增加,GF标准化的远端钠重吸收量增加。Kaliuresis增加。在长达46 d的EDM中,钠滤过电荷减少,低钠血症增强。绝对钠重吸收和相对钠重吸收均因近端和远端而减少。钾利尿增强,无钠水清除率下降。在11天的EDM期间,尿钠损失的增加是由肾小球高滤过引起的,导致小管平衡的功能减弱和肾元远端段的相对功能障碍,强调了RAAS对肾脏离子调节功能的保护作用。fedm发展过程中肾元管状段总重吸收电位的降低反映在近端小管上,而保存的管-管平衡证明了远端小管在26天长的EDM中功能完整。RAAS病理激活和肾小管肾小球反馈对肾血流自我调节的衰减可能是26天四氧嘧啶型糖尿病发生小管疾病的一个起始因素,随后在46天的EDM中进展。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
PECULIARITIES OF IONOREGULATORY RENAL FUNCTION OF RATS IN THE DYNAMICS OF EXPERIMENTAL DIABETES MELLITUS DEVELOPMENT WITH UNDERLYING PHARMACOLOGICAL BLOCADE OF RENIN-ANGIOTENSINALDOSTERONE SYSTEM
The aim of the study – to explore the role of the renin-angiotensin-aldosteronesystem (RAAS) in the disturbance of ionoregulatory renal function in alloxan-inducedexperimental diabetes mellitus (EDM).Material and methods. The experiments were carried out on 78 white non-linearmature male rats with 11-, 26- and 46-day long alloxan-induced EDM with underlyingpharmacological blockade of RAAS by administration of kaptopril. The study ofionoregulating function of the kidneys was provided by the clearance method under thecondition of water 2-hour diuresis.Results. Pharmacological blockade of RAAS in rats with alloxan-induced EDM causedan intensification of natriuresis at all stages of the experiment: increased urinaryconcentration of sodium ions, its excretion and clearance. On the 11th day of EDM, thesodium filtration charge increased with the development of hyponatremia, proximal anddistal sodium reabsorption standardized in volume of glomerular filtrate (GF) decreased,kaliuresis was suppressed, and sodium-free water clearance elevated. In case of 26-daylong EDM, the sodium filtration charge decreased, its absolute and relative reabsorption,the distal sodium reabsorption standardized by GF increased. Kaliuresis increased. In46-day long EDM, the sodium filtration charge decreased, and hyponatremia enhanced.Absolute and relative sodium reabsorption reduced due to both – proximal and distal.Kaliuresis augmented, the clearance of sodium-free water declined.Conclusions. The increase in urinary sodium loss during the 11-day EDM is stipulatedby glomerular hyperfiltration, causing a functional weakening of the tubulotubularbalance and relative dysfunction of the distal segment of the nephron, emphasizing therenoprotective effect of RAAS on ionoregulatory function of the kidneys. The decrease inthe total reabsorption potential of the tubular segment of the nephron in the dynamics ofEDM development reflects on the proximal tubules, and preserved tubulotubular balancecertifies functional intactness of the distal tubules in 26-day long EDM. RAAS pathologicalactivation and attenuation of the renal blood flow autoregulation by tubuloglomerularfeedback may serve as an initiating factor in the development of tubular disorders in 26-day long alloxan diabetes with following progression in 46-day long EDM.
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