Fujii N, Tanaka M, Ohnishi J, Yukawa K, Takimoto E, Shimada S, Naruse M, Sugiyama F, Yagami K, Murakami K
Institute of Applied Biochemistry, Gene Experiment Center, University of Tsukuba, Ibaraki, Japan.
Biochem Biophys Res Commun. 1995 Jul 17;212(2):326-33. doi: 10.1006/bbrc.1995.1973.
Tsukuba hypertensive mice, which carry the human genes for renin and angiotensinogen, show cardiac hypertrophy as well as hypertension due to activation of the renin-angiotensin system (RAS). Here, we compared the cardiac angiotensin II (Ang II) receptor contents in these and normotensive control mice by means of ligand binding studies and competitive reverse transcription-polymerase chain reaction analyses. The content of the Ang II receptor type 1 (AT1) was significantly higher at both the protein (2.5-fold; p < 0.01) and mRNA (1.4-fold; p < 0.05) levels in the hypertensive mice than that in control mice. Almost identical levels of the Ang II receptor type 2 (AT2) expression were identified at the mRNA levels in the two types of mice, although the levels were less than 20% of those of AT1 mRNA in control mice. These results suggest that AT1 in the heart is upregulated in response to Ang II-induced hypertrophic change and that, in particular, the upregulation of AT1 in particular contributes to the development and/or maintenance of cardiac hypertrophy in conjunction with the increase in Ang II production, because AT1 is responsible for cardiac hypertrophy related to the RAS.
携带人肾素和血管紧张素原基因的筑波高血压小鼠，由于肾素 - 血管紧张素系统（RAS）的激活，出现心脏肥大以及高血压。在此，我们通过配体结合研究和竞争性逆转录 - 聚合酶链反应分析，比较了这些高血压小鼠和正常血压对照小鼠心脏中血管紧张素II（Ang II）受体的含量。高血压小鼠中1型血管紧张素II受体（AT1）的含量在蛋白质水平（2.5倍；p < 0.01）和mRNA水平（1.4倍；p < 0.05）均显著高于对照小鼠。在两种类型小鼠的mRNA水平上，鉴定出2型血管紧张素II受体（AT2）的表达水平几乎相同，尽管该水平在对照小鼠中不到AT1 mRNA水平的20%。这些结果表明，心脏中的AT1会因Ang II诱导的肥大变化而上调，特别是AT1的上调尤其与Ang II产生增加一起，对心脏肥大的发展和/或维持有贡献，因为AT1与RAS相关的心脏肥大有关。
