Literature DB >> 21256551

Angiotensin type-1 receptor blocker candesartan inhibits calcium oxalate crystal deposition in ethylene glycol-treated rat kidneys.

Iwao Yoshioka1, Masao Tsujihata, Wongswat Akanae, Norio Nonomura, Akihiko Okuyama.   

Abstract

OBJECTIVES: To investigate whether an angiotensin type-1 receptor blocker could inhibit calcium oxalate crystal deposition using ethylene glycol-treated rats. The renoprotective effect has been reported to be another role of angiotensin type-1 receptor blockers in addition to their role in lowering blood pressure. Recent research has suggested that inhibiting reactive oxidative species generation and tubulointerstitial inflammation is the major role of angiotensin type-1 receptor blockers. These 2 factors are also important in the mechanism of calcium oxalate stone formation.
METHODS: We divided 28 rats, aged 7 weeks, into 4 groups: group 1, control rats; group 2, candesartan-treated rats; group 3, stone-forming rats; and group 4, candesartan-treated stone-forming rats. The kidney crystal deposits were examined, and the oxidative stress biomarker, nicotinamide adenine dinucleotide phosphate oxidase activity, general and urinary variables, and the transforming growth factor-β level in kidney tissue were compared among the 4 groups.
RESULTS: The candesartan-treated rats were healthy and had weight gain similar to that of the control rats, although a significant reduction in blood pressure was observed. The urinary components associated with calcium oxalate stone formation were not influenced by candesartan treatment; however, significantly fewer crystal deposits were observed in group 4. The oxidative biomarker and nicotinamide adenine dinucleotide phosphate oxidase activity decreased, and the level of transforming growth factor-β was suppressed in group 4.
CONCLUSIONS: Candesartan had substantial effects on crystal formation in the rat kidney by suppressing nicotinamide adenine dinucleotide phosphate oxidase and the transforming growth factor-β levels.
Copyright © 2011 Elsevier Inc. All rights reserved.

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Year:  2011        PMID: 21256551     DOI: 10.1016/j.urology.2010.11.019

Source DB:  PubMed          Journal:  Urology        ISSN: 0090-4295            Impact factor:   2.649


  8 in total

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Authors:  Nahla E El-Ashmawy; Hoda A El-Bahrawy; Heba H Ashmawy; Eman G Khedr
Journal:  PLoS One       Date:  2021-05-13       Impact factor: 3.240

2.  Selective Rac1 inhibition protects renal tubular epithelial cells from oxalate-induced NADPH oxidase-mediated oxidative cell injury.

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3.  Why does atorvastatin inhibit renal crystal retention?

Authors:  Masao Tsujihata; Iwao Yoshioka; Akira Tsujimura; Norio Nonomura; Akihiko Okuyama
Journal:  Urol Res       Date:  2011-03-12

4.  Total flavonoids of Desmodium styracifolium attenuates the formation of hydroxy-L-proline-induced calcium oxalate urolithiasis in rats.

Authors:  Jianfu Zhou; Jing Jin; Xiong Li; Zhongxiang Zhao; Lei Zhang; Qian Wang; Jing Li; Qiuhong Zhang; Songtao Xiang
Journal:  Urolithiasis       Date:  2017-05-31       Impact factor: 3.436

5.  Label-free quantitative proteomics reveals differentially regulated proteins influencing urolithiasis.

Authors:  C A Wright; S Howles; D C Trudgian; B M Kessler; J M Reynard; J G Noble; F C Hamdy; B W Turney
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Authors:  Vincent de Kemp; Petra de Graaf; Joost O Fledderus; J L H Ruud Bosch; Laetitia M O de Kort
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7.  Losartan Ameliorates Calcium Oxalate-Induced Elevation of Stone-Related Proteins in Renal Tubular Cells by Inhibiting NADPH Oxidase and Oxidative Stress.

Authors:  Baolong Qin; Qing Wang; Yuchao Lu; Cong Li; Henglong Hu; Jiaqiao Zhang; Yufeng Wang; Jianning Zhu; Yunpeng Zhu; Yang Xun; Shaogang Wang
Journal:  Oxid Med Cell Longev       Date:  2018-04-24       Impact factor: 6.543

8.  Pyrrosia petiolosa Extract Ameliorates Ethylene Glycol-Induced Urolithiasis in Rats by Inhibiting Oxidative Stress and Inflammatory Response.

Authors:  Fangmin Zhou; Xingshan Wang
Journal:  Dis Markers       Date:  2022-08-05       Impact factor: 3.464

  8 in total

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