A large body of evidence supports the presence of local production of angiotensins in the kidney. It is widely believed that renin-angiotensin system (RAS) blockers, through interference with such production and/or the local effects of angiotensin (Ang) II, exert protective renal effects. Yet, whether such production affects blood pressure independently from the circulating RAS is still a matter of debate. To investigate this, a recent study by Gonzalez-Villalobos et al. (J Clin Invest 2013; 123: 2011-2023) has studied the consequences of infusing Ang II or the nitric oxide synthase inhibitor L-NAME in mice lacking renal angiotensin-converting enzyme (ACE). They observed blunted blood pressure and renal responses in the renal ACE knockout mice versus wild-type controls. This review discusses to what degree these findings can be considered as unequivocal evidence for ACE-mediated Ang II formation in the kidney as an independent determinant of hypertension.

ACE inhibitor, Angiotensin, Chymase, Diabetes, Hypertension, Renin
dx.doi.org/10.1093/ndt/gft333, hdl.handle.net/1765/61654
Nephrology, Dialysis, Transplantation
Department of Cardio-Thoracic Surgery

Lu, X, Roksnoer, L.C.W, & Danser, A.H.J. (2013). The intrarenal renin-angiotensin system: Does it exist? Implications from a recent study in renal angiotensin-converting enzyme knockout mice. Nephrology, Dialysis, Transplantation (Vol. 28, pp. 2977–2982). doi:10.1093/ndt/gft333