Abstract 187: The Absence of Renal ACE Blunts the Renal Response and the Hypertension Induced by Nitric Oxide Synthesis Inhibition

• Published in: Hypertension (Dallas, Tex. 1979) Tex. 1979), 2013-09, Vol.62 (suppl_1)
• Main Authors: Giani, Jorge F, Janjoulia, Tea, Kamat, Nikhil, Peti-Peterdi, Janos, Toblli, Jorge E, Bernstein, Kenneth E, McDonough, Alicia A, Gonzalez-Villalobos, Romer A
• Format: Article
• Language: English
• ISSN: 0194-911X; 1524-4563
• DOI: 10.1161/hyp.62.suppl_1.A187

Abstract only We previously showed that the responses to angiotensin (Ang) II infusion observed in wild type (WT) mice were effectively prevented in mice lacking renal ACE (ACE 3/3 and ACE 10/10 mice) including: hypertension, renal Ang II accumulation, sodium and water retention, and activation of ion transporters in the loop of Henle (NKCC2) and distal nephron (NCC, ENaC, and pendrin). The aim of this study was to test if the absence of renal ACE also protects against hypertension induced by nitric oxide (NO) synthesis inhibition with L-NAME, a low-plasma Ang II hypertension model associated with renal renin-angiotensin system (RAS) activation. In response to L-NAME (0.5 mg/mL in drinking water, 4 wk; n=12-17), systolic blood pressure (SBP) of WT rose from 110±2 to 135±3 mmHg (p