Increased AT(1) receptor expression and mRNA in kidney glomeruli of AT(2) receptor gene-disrupted mice.
Increased AT(1) receptor expression and mRNA in kidney glomeruli of AT(2) receptor gene-disrupted mice.
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AT(2) 受体基因破坏小鼠肾小球中 AT(1) 受体表达和 mRNA 增加。
DOI:
10.1152/ajprenal.2001.280.1.f71
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发表时间:
2001
期刊:
影响因子:
--
通讯作者:
Armando,I
中科院分区:
文献类型:
--
作者:
Saavedra,JM;Hauser,W;Ciuffo,G;Egidy,G;Hoe,KL;Johren,O;Sembonmatsu,T;Inagami,T;Armando,I
The proposed feedback between angiotensin II AT2and AT1receptors prompted us to study AT1receptor expression in kidneys of male AT2receptor-gene disrupted mice (agtr2−/y). In wild-type (agtr2+/y) mice, AT1receptor binding and mRNA is abundant in glomeruli, and AT1receptor binding is also high in the inner stripe of the outer medulla. AT2receptors are scarce, primarily associated to cortical vascular structures. Inagtr2−/y mice, AT1receptor binding and mRNA were increased in the kidney glomeruli, and AT1receptor binding was higher in the rest of the cortex and outer stripe of the outer medulla, but not in its inner stripe, indicating different cellular regulation. Although AT2receptor expression is very low in maleagtr 2+/y mice, their gene disruption alters AT1receptor expression. AT1upregulation alone may explain the AT2gene-disrupted mice phenotype such as increased blood pressure, higher sensitivity to angiotensin II, and altered renal function. The indirect AT1/AT2receptor feedback could have clinical significance because AT1antagonists are widely used in medical practice.