在这个为期6周的研究的每一天期间,研究者们都注射盐水或血管紧张素1 - 7肽到生长人类肺癌的小鼠里。
Every day during the six-week study, researchers injected either saline or the angiotensin (1-7) peptide into mice growing human lung cancer tumors.
来自澳大利亚的MichaelMathai及她的同事研究了血管紧张素转换酶基因敲除小鼠,该基因编码肾素-血管紧张素系统中一种关键蛋白。
Michael Mathai and colleagues in Australia examined mice that were missing a gene that encodes for angiotensin-converting enzyme, a key protein for the renin-angiotensin system.
虽然小剂量的血管紧张素II注射对雄性小鼠血压没有影响,但却能显著减低雌鼠的平均动脉压,而此现象能够被血管紧张素受体拮抗剂PD123319所阻断。
Although this low dose had no effect on MAP in the male, it significantly decreased MAP in the female, and this effect was prevented by coinfusing the animals with PD123319, an antagonist of the AT2R.
依据上述论点,本研究利用AT2受体基因敲出小鼠,观察了AT2受体缺失后是否造成肾素-血管紧张素系统其它成分代偿性紊乱。
In the present study, we investigated whether gene deletion of AT2 receptor causes the compensatory chaos of renin-angiotensin system in mice.
依据上述论点,本研究利用AT2受体基因敲出小鼠,观察了AT2受体缺失后是否造成肾素-血管紧张素系统其它成分代偿性紊乱。
In the present study, we investigated whether gene deletion of AT2 receptor causes the compensatory chaos of renin-angiotensin system in mice.
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