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对同源性肾素Dahl盐敏感大鼠肾素-血管紧张素系统的评估。

Evaluation of the renin-angiotensin system in a congenic renin Dahl salt-sensitive rat.

作者信息

DiPaola N R, Rapp J P, Brand P H, Beierwaltes W H, Metting P J, Britton S L

机构信息

Department of Physiology and Molecular Medicine, Medical College of Ohio, Toledo 43699-0008, USA.

出版信息

Genes Funct. 1997 Jun;1(3):215-26. doi: 10.1046/j.1365-4624.1997.00017.x.

DOI:10.1046/j.1365-4624.1997.00017.x
PMID:9680296
Abstract

When an approximately 30 centiMorgan (cM) region of chromosome 13 containing the renin gene from the Dahl salt-resistant rat (R) was introgressed into the Dahl salt-sensitive rat (S), the resulting congenic rat (designated S.R-Ren) had a systolic blood pressure on a 2% (w/w) salt diet that was 24 mmHg lower than that of its S counterpart. Due to the large size of the transferred segment (over 30 million bp), the question remained as to whether or not the renin gene was the cause of the blood-pressure difference between the strains. We evaluated the role of the renin-angiotensin system in S.R-Ren and S rats fed a 0.05% salt diet by examining differences between strains in (1) expression of renin in three tissue types, (2) the blood-pressure response to blockade of both angiotensin-converting enzyme and angiotensin II receptors, and (3) pressure natriuresis. No differences were found in renin levels in plasma, kidney or adrenal gland between strains. The blood-pressure responses to the angiotensin-converting-enzyme inhibitor captopril and to the angiotensin II-receptor blocker saralasin in conscious S and S.R-Ren rats were similar. Furthermore, renal function, evaluated by a pressure-natriuresis index that took into account both the time and the arterial pressure needed to excrete an acute salt load, did not differ between strains. Our findings therefore fail to demonstrate a role for the renin gene in conferring lower blood pressure in the congenic rat and suggest that there is an unknown arterial-pressure-regulating locus in this 30 cM region of chromosome 13.

摘要

当将来自 Dahl 盐抵抗大鼠(R)的包含肾素基因的 13 号染色体上大约 30 厘摩(cM)的区域导入 Dahl 盐敏感大鼠(S)时,所产生的近交系大鼠(命名为 S.R-Ren)在 2%(w/w)盐饮食下的收缩压比其 S 品系对应大鼠低 24 mmHg。由于转移片段的尺寸较大(超过 3000 万碱基对),肾素基因是否是品系间血压差异的原因这一问题仍然存在。我们通过检查品系间在以下方面的差异,评估了肾素 - 血管紧张素系统在喂食 0.05%盐饮食的 S.R-Ren 和 S 大鼠中的作用:(1)三种组织类型中肾素的表达;(2)对血管紧张素转换酶和血管紧张素 II 受体阻断的血压反应;(3)压力利尿。品系间血浆、肾脏或肾上腺中的肾素水平未发现差异。清醒的 S 和 S.R-Ren 大鼠对血管紧张素转换酶抑制剂卡托普利和血管紧张素 II 受体阻滞剂沙拉新的血压反应相似。此外,通过考虑排泄急性盐负荷所需的时间和动脉压的压力利尿指数评估的肾功能,品系间没有差异。因此,我们的研究结果未能证明肾素基因在赋予近交系大鼠较低血压方面的作用,并表明在 13 号染色体的这个 30 cM 区域存在一个未知的动脉血压调节基因座。

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