BEHAVIORAL AND CARDIOVASCULAR EFFECTS OF DISRUPTING THE ANGIOTENSIN-II TYPE-2 RECEPTOR GENE IN MICE
BEHAVIORAL AND CARDIOVASCULAR EFFECTS OF DISRUPTING THE ANGIOTENSIN-II TYPE-2 RECEPTOR GENE IN MICE
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DOI：
10.1038/377744a0
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发表时间：
1995-10-26
期刊：
影响因子：
64.8
通讯作者：
KOBILKA, BK
中科院分区：
文献类型：
--
作者：
HEIN, L;BARSH, GS;KOBILKA, BK
血管紧张素 II 是血压以及水和电解质平衡的有效调节剂，可与两种不同的 G 蛋白偶联受体结合。 1 型受体 (AT(1)) 介导血管紧张素 II 的血管加压和醛固酮分泌作用，但 2 型受体 (AT(2)；参考文献 1, 2) 的功能尚不清楚，尽管它在成人 (3) 和胚胎 (4) 生命中都有表达。为了解决这个问题，我们培育了缺乏编码 AT(2) 受体基因的小鼠。突变小鼠发育正常，但对缺水的饮水反应受损，自发运动减少。他们的基线血压正常，但注射血管紧张素 II 后血管加压反应增加。因此，虽然AT(2)受体不是胚胎发育所必需的，但它在肾素-血管紧张素系统介导的中枢神经系统和心血管功能中发挥作用。
ANGIOTENSIN II, a potent regulator of blood pressure and of water and electrolyte balance, binds to two different G-protein-coupled receptors. The type-1 receptor (AT(1)) mediates the vasopressive and aldosterone-secreting effects of angiotensin II, but the function of the type-2 receptor (AT(2); refs 1, 2) is unknown, although it is expressed in both adult(3) and embryonic(4) life. To address this question, we have generated mice lacking the gene encoding the AT(2) receptor. Mutant mice develop normally, but have an impaired drinking response to water deprivatian as well as a reduction in spontaneous movements. Their baseline blood pressure is normal, but they show an increased vasopressor response to injection of angiotensin II. Thus, although the AT(2) receptor is not required for embryonic development, it plays a role in the central nervous system and cardiovascular functions that are mediated by the renin-angiotensin system.