期刊论文详细信息
Cardiorenal medicine
Vascular Calcification Exacerbates Abnormal Blood Pressure Variability in Chronic Kidney Disease: A “Two-Step” Study in Rats
article
Li, Yupei1  Su, Baihai1  Xiong, Yuqin2  Yu, Yang1  Huang, Ke3  Liao, Ruoxi1  Wang, Liya1  Zhang, Zhuyun1  Li, Jiameng1  Qin, Zheng1  Sun, Si2 
[1] Department of Nephrology, West China Hospital, Sichuan University;Department of Nephrology, West China School of Public Health and West China Fourth Hospital, Sichuan University;West China School of Medicine, Sichuan University
关键词: Vascular calcification;    Blood pressure variability;    Chronic kidney disease;    Animal models of CKD-VC;   
DOI  :  10.1159/000528898
学科分类:心脏病和心血管学
来源: S Karger AG
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【 摘 要 】

Introduction: Vascular calcification (VC) is a common complication of chronic kidney disease (CKD) with poor cardiovascular prognosis. The aim of this study was to explore the impact of VC on blood pressure variability (BPV) in animal models of CKD. Methods: Two optimal modelling methods, adenine high-phosphorus (HP) diet + calcitriol and 5/6 nephrectomy (Nx) + HP diet + calcitriol, for CKD-VC were chosen from the first-step experiment for the next step. A total of 36 male Wistar rats were randomly assigned to the standard-chow, sham-operated, adenine, 5/6Nx, adenine-VC, and 5/6Nx-VC groups. Continuous blood pressure (BP) measurement using the BP-2000 animal noninvasive BP analyser was started at the 9th week for the standard-chow, adenine, and adenine-VC groups and at the 7th week for the sham-operated, 5/6Nx, and 5/6Nx-VC groups. BPV metrics (BPVs), including the difference between maximum and minimum values, standard deviation, coefficient of variation, average real variability, and residuals derived from the generalized linear model of BP, were calculated. Results: The first experiment showed that the use of calcitriol accelerated the progression of VC in CKD rats (the modelling period was shortened from 16 weeks to 4–8 weeks) and confirmed the occurrence of VC at weeks 8 and 6 in the adenine-VC and 5/6Nx-VC groups, respectively. In the second experiment, 13 of 20 hour-to-hour BPVs increased significantly with the development of CKD and VC. BPV differences among the standard-chow, adenine, and adenine-VC groups were mainly due to the differences between the standard-chow and adenine-VC groups (7 of 10 BPVs were significantly different), followed by the differences between the standard-chow and adenine groups (3 of 10). BPV differences among the sham-operated, 5/6Nx, and 5/6Nx-VC groups were caused by the differences between the 5/6Nx-VC and 5/6Nx groups (4 of 10) or the 5/6Nx-VC and sham-operated groups (3 of 10). Conclusion: An increased BPV is observed in CKD rats, and VC further aggravates the abnormality of BPVs independent of CKD.

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