| First Author | Cole JM | Year | 2003 |
| Journal | Hypertension | Volume | 41 |
| Issue | 2 | Pages | 313-21 |
| PubMed ID | 12574101 | Mgi Jnum | J:103086 |
| Mgi Id | MGI:3608444 | Doi | 10.1161/01.hyp.0000050650.52007.83 |
| Citation | Cole JM, et al. (2003) Mice lacking endothelial ACE: normal blood pressure with elevated angiotensin II. Hypertension 41(2):313-21 |
| abstractText | Recently, the concept of local renin-angiotensin systems (RAS) capable of generating angiotensin II apart from the circulation has received considerable attention. To investigate this, we generated ACE 1/3 mice in which one allele of ACE is null and the second allele was engineered to express ACE on the surface of hepatocytes. ACE 1/3 mice express no endothelial ACE and lack ACE within the lungs. Their kidneys contain <7.8% the enzyme levels present in control mice. Plasma conversion of angiotensin I to angiotensin II was 43.3% normal. The baseline blood pressure and renal function of the ACE 1/3 mice were normal, probably as a function of a marked increase of both plasma angiotensin I and angiotensin II. When exposed to 2 weeks of a salt-free diet (a stress diet stimulating the RAS), blood pressure in ACE 1/3 mice decreased to 92.3+/-2.0 mm Hg, a level significantly lower than that of wild-type control mice. The ACE 1/3 mice demonstrate the plasticity of the RAS and show that significant compensation is required to maintain normal, basal blood pressure in a mouse with an impaired local vascular and renal RAS. |
