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Angiotensin II receptor blockade does not improve left ventricular function andremodeling in subacute mitral regurgitation in the dog

Gilbert J. Perry, MD^*, Chih-Chang Wei, PhD^*, Gerald H. Hankes, DVM, PhD, S. Ray Dillon, DVM, Patricia Rynders, DVM, Rupak Mukherjee, PhD, Francis G. Spinale, MD, PhD and Louis J. Dell’Italia, MD^*,*

^* Birmingham Veterans Affairs Medical Center, University of Alabama, Department of Medicine, Division of Cardiovascular Disease, Birmingham, Alabama, USA
Auburn College of Veterinary Medicine, Auburn, Alabama, USA
Department of Surgery, Medical University of South Carolina, Charleston, South Carolina, USA

View larger version (12K): [in a new window]   Figure 1 Plasma renin activity: angiotensin (ANG) I and ANG II levels are increased in mitral regurgitation (MR) and MR+AT1RB compared to normal (NL) dogs. *p < 0.01 MR+AT1RB and MR vs. normal dogs. AT1RB = angiotensin II type-1 receptor blocker.

View larger version (13K): [in a new window]   Figure 2 Left ventricular (LV) angiotensin (ANG) II concentrations and LV angiotensin-converting enzyme (ACE) activity levels in normal, mitral regurgitation (MR) and MR+AT1RB dogs demonstrating that ANG II and ACE were increased greater than twofold in MR dogs vs. normals, but were normalized by AT1RB. *p < 0.05 MR vs. normal dogs. AT1RB = angiotensin II type-1 receptor blocker.