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肾尿紧张素II系统在 Dahl 盐抵抗大鼠血压调节中发挥作用。

Renal Urotensin II System Plays Roles in the Regulation of Blood Pressure in Dahl Salt-Resistant Rat.

作者信息

Wu Fei, Chen Guanjong, Zhang Aihua, Yu Yang, Fan Minhua, Tang Chaoshu

机构信息

Department of Nephrology, Peking University Third Hospital, Beijing, China.

Department of Gynecology and Obstetrics, Peking University Third Hospital, Beijing, China.

出版信息

Int J Hypertens. 2016;2016:9146870. doi: 10.1155/2016/9146870. Epub 2016 Dec 19.

DOI:10.1155/2016/9146870
PMID:28097020
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5209633/
Abstract

. Dahl salt-resistant (SR) animal models are similar to peritoneal dialysis patients with fluid volumes overload with normal blood pressure in hemodynamic profiles. We will verify the roles of UII in the regulation of blood pressure in these animal models. . The Dahl salt-sensitive (SS) and SR rats and UII receptor gene knocked out (KO) mice were placed on a high-salt diet. Renal tissues were performed for the expression of UII in Dahl groups. . After high-salt diet for 6 weeks, the systolic blood pressure (SBP) in SR group was significantly lower, accompanied with higher urinary UII levels, higher 24-hour urinary sodium excretion, and higher urinary creatinine clearance in the SR rats in comparison to SS group. The expressions of UII and UT were both upregulated in the kidney tissues of SR group in comparison to SS group ( < 0.05). After high-salt diet for 8 weeks, the SBP of the KO group is significantly higher than that of the wild type group. . We first demonstrate that renal UII system can play important roles in the regulation of blood pressure in Dahl SR rats which can be highly correlated to its effect on renal tubular sodium absorption.

摘要

达利盐抵抗(SR)动物模型在血流动力学特征上与伴有血容量超负荷且血压正常的腹膜透析患者相似。我们将在这些动物模型中验证尾加压素II(UII)在血压调节中的作用。. 将达利盐敏感(SS)大鼠、SR大鼠和UII受体基因敲除(KO)小鼠置于高盐饮食中。对达利组的肾脏组织进行UII表达检测。. 高盐饮食6周后,与SS组相比,SR组大鼠的收缩压(SBP)显著降低,同时尿UII水平升高、24小时尿钠排泄增加以及尿肌酐清除率升高。与SS组相比,SR组肾脏组织中UII和尾加压素受体(UT)的表达均上调(<0.05)。高盐饮食8周后,KO组的SBP显著高于野生型组。. 我们首次证明,肾脏UII系统在达利SR大鼠的血压调节中发挥重要作用,这可能与其对肾小管钠重吸收的影响高度相关。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2316/5209633/76b0063b6280/IJHY2016-9146870.008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2316/5209633/d771e68bd715/IJHY2016-9146870.001.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2316/5209633/45ab7d92be51/IJHY2016-9146870.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2316/5209633/5a75a90e6539/IJHY2016-9146870.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2316/5209633/2d1c3f76d50a/IJHY2016-9146870.006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2316/5209633/18db26d700b9/IJHY2016-9146870.007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2316/5209633/76b0063b6280/IJHY2016-9146870.008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2316/5209633/d771e68bd715/IJHY2016-9146870.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2316/5209633/3f0eac118612/IJHY2016-9146870.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2316/5209633/6a56f9de2473/IJHY2016-9146870.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2316/5209633/45ab7d92be51/IJHY2016-9146870.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2316/5209633/5a75a90e6539/IJHY2016-9146870.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2316/5209633/2d1c3f76d50a/IJHY2016-9146870.006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2316/5209633/18db26d700b9/IJHY2016-9146870.007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2316/5209633/76b0063b6280/IJHY2016-9146870.008.jpg

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本文引用的文献

1
Urotensin II Induces ER Stress and EMT and Increase Extracellular Matrix Production in Renal Tubular Epithelial Cell in Early Diabetic Mice.尾加压素II诱导早期糖尿病小鼠肾小管上皮细胞内质网应激和上皮-间质转化并增加细胞外基质生成
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Ontogeny of the renal urotensin II system in the rat.
大鼠肾脏尾加压素 II 系统的个体发生。
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