摘要
Renin angiotensin system （RAS） activation has a significant influence on renal disease progression. The classical angiotensin-converting enzyme （ACE）-angio-tensin Ⅱ （Ang Ⅱ）-Ang Ⅱ type 1 （AT1） axis is considered to control the effects of RAS activation on renal disease. However, since its discovery in 2000 ACE2 has also been demonstrated to have a significant impact on the RAS. The synthesis and catabolism of Ang Ⅱ are regulated via a complex series of interactions, which involve ACE and ACE2. In the kidneys, ACE2 is expressed in the proximal tubules and less strongly in the glomeruli. The synthesis of inactive Ang 1-9 from Ang Ⅰ and the catabolism of Ang Ⅱ to produce Ang 1-7 are the main functions of ACE2. Ang 1-7 reduces vasoconstriction, water retention, salt intake, cell proliferation, and reactive oxygen stress, and also has a renoprotective effect. Thus, in the non-classical RAS the ACE2-Ang 1-7-Mas axis counteracts the ACE-Ang Ⅱ-AT1 axis. This review examines recent human and animal studies about renal ACE and ACE2.
Renin angiotensin system(RAS) activation has a significant influence on renal disease progression. The classical angiotensin-converting enzyme(ACE)-angiotensin Ⅱ(Ang Ⅱ)-Ang Ⅱ type 1(AT1) axis is considered to control the effects of RAS activation on renal disease.However, since its discovery in 2000 ACE2 has also been demonstrated to have a significant impact on the RAS.The synthesis and catabolism of Ang Ⅱ are regulated via a complex series of interactions, which involve ACE and ACE2. In the kidneys, ACE2 is expressed in the proxima tubules and less strongly in the glomeruli. The synthesisof inactive Ang 1-9 from Ang Ⅰ and the catabolism of Ang Ⅱ to produce Ang 1-7 are the main functions of ACE2. Ang 1-7 reduces vasoconstriction, water retention, salt intake, cell proliferation, and reactive oxygen stress, and also has a renoprotective effect. Thus, in the nonclassical RAS the ACE2-Ang 1-7-Mas axis counteracts the ACE-Ang Ⅱ-AT1 axis. This review examines recent human and animal studies about renal ACE and ACE2.
基金
Supported by The Toho University School of Medicine Research Foundation
