Auzan Colette, Clauser Eric
Département d'Endocrinologie, Métabolisme et Cancer, Intitut Cochin, INSERM U567-UMR 8104 CNRS, Université Paris Descartes, Faculté de Médecine Cochin, 24 rue du faubourg St. acques, 75014 Paris, France.
J Soc Biol. 2009;203(4):295-302. doi: 10.1051/jbio/2009033. Epub 2010 Feb 1.
Angiotensin II AT1 receptor is a G protein coupled receptor, which transduces the physiological effects (vasoconstriction, aldosterone secretion) f this vasoactive peptide. On an evolutionary point of view, this receptor has appeared early in the development of vertebrates, since it is present in cartilagenous fish. It has been duplicated in rodents without any consequence on its functions. It is unlikely that the angiotensin AT2 receptor, whose functions are still debated, has diverged from a common ancestral angiotensin receptor with the AT1 receptor. Numerous activating or inactivating point mutations have been identified by site-directed mutagenesis of the AT1 receptor sequence. However, such natural mutations do not appear to be frequent in the genesis of human diseases or in the diversity of phenotypic traits.
血管紧张素II AT1受体是一种G蛋白偶联受体，它可传导这种血管活性肽的生理效应（血管收缩、醛固酮分泌）。从进化的角度来看，这种受体在脊椎动物发育早期就已出现，因为在软骨鱼中就有存在。它在啮齿动物中发生了复制，但对其功能没有任何影响。血管紧张素AT2受体的功能仍存在争议，它不太可能与AT1受体源自共同的血管紧张素受体祖先。通过对AT1受体序列进行定点诱变，已鉴定出许多激活或失活的点突变。然而，这种自然突变在人类疾病的发生或表型特征的多样性中似乎并不常见。
