Suppr超能文献

环磷酸鸟苷诱导的心肌细胞功能降低部分是由肌浆网Ca(2+) -ATP酶的激活介导的。

Cyclic GMP-induced reduction in cardiac myocyte function is partially mediated by activation of the sarcoplasmic reticulum Ca(2+)-ATPase.

作者信息

Zhang Qihang, Yan Lin, Weiss Harvey R, Scholz Peter M

机构信息

Heart and Brain Circulation Laboratory, Department of Physiology and Biophysics, Robert Wood Johnson Medical School, University of Medicine and Dentistry of New Jersey, One Robert Wood Johnson Place, New Brunswick, N.J. 08903-0019, USA.

出版信息

Pharmacology. 2002 Feb;64(2):106-12. doi: 10.1159/000056158.

Abstract

We tested the hypothesis that the mechanism through which cyclic GMP reduces cardiac function is mediated by activation of the sarcoplasmic reticulum Ca(2+)-ATPase (SERCA). Cardiac myocytes were isolated from New Zealand white rabbits (n = 11). Individual ventricular cells were stimulated by electrical field stimulation. The maximal rate of cell shortening and percentage shortening were measured with a video edge detector. Thapsigargin (10(-8) mol/l) was used as a specific inhibitor of SERCA. When 8-bromo-cyclic GMP (8-Br-cGMP, 10(-7, -6, -5) mol/l) was added to cells, the maximal rate of myocyte shortening (R(max), microm/s) and percentage shortening were both decreased in a concentration-dependent manner. R(max) decreased 27% from 117 +/- 12 at baseline to 85.2 +/- 13 when 10(-5) mol/l of 8-Br-cGMP was present, and percent shortening was reduced 28% from 6.0 +/- 0.5 to 4.3 +/- 0.5%. Thapsigargin (10(-8) mol/l) increased the maximal rate of myocyte shortening and percent shortening. Addition of thapsigargin prior to 8-Br-cGMP reduced the negative effects of cGMP on myocyte function. The percent shortening decreased only 11% and R(max) decreased 14% with 10(-5) mol/l 8-Br-cGMP, which was not significant. Cyclopiazonic acid, another SERCA inhibitor, was also used to test whether 8-Br-cGMP reduced myocyte function through SERCA. The results were similar to those when thapsigargin was used. These results indicated that the cyclic GMP-induced reduction in cardiac myocyte function was partially mediated through the action of the sarcoplasmic reticulum Ca(2+)-ATPase.

摘要

我们验证了如下假设

环磷酸鸟苷(cGMP)降低心脏功能的机制是由肌浆网Ca(2+) -ATP酶(SERCA)的激活介导的。从新西兰白兔(n = 11)分离出心肌细胞。通过电场刺激单个心室细胞。用视频边缘检测器测量细胞缩短的最大速率和缩短百分比。毒胡萝卜素(10(-8) mol/l)用作SERCA的特异性抑制剂。当向细胞中加入8-溴环磷酸鸟苷(8-Br-cGMP,10(-7, -6, -5) mol/l)时,心肌细胞缩短的最大速率(R(max),微米/秒)和缩短百分比均呈浓度依赖性降低。当存在10(-5) mol/l的8-Br-cGMP时,R(max)从基线时的117±12降低27%至85.2±13,缩短百分比从6.0±0.5降低28%至4.3±0.5%。毒胡萝卜素(10(-8) mol/l)增加了心肌细胞缩短的最大速率和缩短百分比。在加入8-Br-cGMP之前添加毒胡萝卜素可降低cGMP对心肌细胞功能的负面影响。对于10(-5) mol/l的8-Br-cGMP,缩短百分比仅降低11%,R(max)降低14%,差异不显著。另一种SERCA抑制剂环匹阿尼酸也用于测试8-Br-cGMP是否通过SERCA降低心肌细胞功能。结果与使用毒胡萝卜素时相似。这些结果表明,环磷酸鸟苷诱导的心肌细胞功能降低部分是通过肌浆网Ca(2+) -ATP酶的作用介导的。

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍。

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

文档翻译

学术文献翻译模型,支持多种主流文档格式。

立即体验