• 主题
高级搜索  >
历史搜索 清空历史
首页> 美国卫生研究院文献>Proceedings of the National Academy of Sciences of the United States of America >Tonic stimulation of renin gene expression by nitric oxide is counteracted by tonic inhibition through angiotensin II.
【2h】

Tonic stimulation of renin gene expression by nitric oxide is counteracted by tonic inhibition through angiotensin II.

机译：一氧化氮对肾素基因表达的滋补刺激被通过血管紧张素II的滋补抑制所抵消。

代理获取
本网站仅为用户提供外文OA文献查询和代理获取服务，本网站没有原文。下单后我们将采用程序或人工为您竭诚获取高质量的原文，但由于OA文献来源多样且变更频繁，仍可能出现获取不到、文献不完整或与标题不符等情况，如果获取不到我们将提供退款服务。请知悉。
页面导航
  • 摘要
  • 著录项
  • 相似文献
  • 相关主题

摘要

This study was designed to examine the possible involvement of prostaglandins and nitric oxide (NO) in the renin stimulatory effect of angiotensin II (AngII) antagonists. To this end, plasma renin activities (PRAs) and renal renin mRNA levels were assayed in rats that were treated with the Ang-converting enzyme inhibitor ramipril or with the AngII AT1-receptor antagonist losartan. Ramipril and losartan increased PRA values from 7.5 +/- 1.6 to 86 +/- 6 and 78 +/- 22 ng of AngI per h per ml and renin mRNA levels from 112 +/- 9% to 391 +/- 20% and 317 +/- 10%, respectively. Inhibition of prostaglandin formation with indomethacin did not influence basal or ramipril-affected PRA. Basal renin mRNA levels also were unchanged by indomethacin, while increases in renin mRNA levels after ramipril treatment were slightly reduced by indomethacin. Inhibition of NO synthase by nitro-L-arginine methyl ester (L-NAME) reduced PRA values to 3.2 +/- 0.9, 34 +/- 13, and 12.1 +/- 2.7 ng of AngI per h per ml in control, ramipril-treated, and losartan-treated animals, respectively. Renin mRNA levels were reduced to 77 +/- 14% under basal conditions and ramipril- and losartan-induced increases in renin mRNA levels were completely blunted after addition of L-NAME. The AngII antagonists, furthermore, induced an upstream recruitment of renin-expressing cells in the renal afferent arterioles, which was also blunted by L-NAME. These findings suggest that renin mRNA levels are tonically increased by NO and that the action of NO is counteracted by AngII.
机译：这项研究旨在检查前列腺素和一氧化氮（NO）可能与血管紧张素II（AngII）拮抗剂的肾素刺激作用有关。为此，在用Ang转化酶抑制剂雷米普利或AngII AT1受体拮抗剂洛沙坦治疗的大鼠中测定血浆肾素活性（PRA）和肾素mRNA水平。雷米普利和氯沙坦使PRA值从7.5 +/- 1.6增至86 +/- 6和78 +/- 22 ng / h / ml，肾素mRNA水平从112 +/- 9％增至391 +/- 20％，分别为317 +/- 10％。吲哚美辛抑制前列腺素的形成并不影响基础或雷米普利影响的PRA。吲哚美辛也未改变基础肾素mRNA水平，而吲哚美辛则使雷米普利治疗后肾素mRNA水平升高略有下降。在对照品雷米普利中，硝基-L-精氨酸甲酯（L-NAME）对NO合酶的抑制将PRA值降至每毫升每小时3.2 +/- 0.9、34 +/- 13和12.1 +/- 2.7 ng AngI每毫升处理的动物和氯沙坦处理的动物。在基础条件下，肾素mRNA水平降低至77 +/- 14％，加入L-NAME后，雷米普利和氯沙坦诱导的肾素mRNA水平升高完全减弱。此外，AngII拮抗剂诱导了肾传入小动脉中肾素表达细胞的上游募集，其也被L-NAME抑制。这些发现表明，NO使肾素mRNA水平升高，而AngII抵消了NO的作用。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
代理获取

客服邮箱：kefu@zhangqiaokeyan.com

京公网安备：11010802029741号 ICP备案号：京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有

  • 客服微信

  • 服务号