Minimally invasive transverse aortic banding (MTAB) is a model for inducing ventricular dysfunction that has been used exclusively in mice. Our objective was to test the efficacy of the MTAB model in rats by using the Sprague Dawley, Dahl salt‐sensitive hypertensive and the recently developed Mas receptor knock out rat. The Mas receptor mediates the physiological effects of the angiotensin peptide ANG1‐7 and thus modulates cardiovascular function. A rat knockout of the Mas1 receptor was generated using zinc‐finger nuclease (ZFN) mediated engineering on the SS genetic background. A 10‐bp deletion in exon1 of the Mas1 gene led to a severely truncated protein and a loss of function. Cardiac function was assessed following MTAB using cardiac ultrasound, PV loop analysis, and histology.Weekly echocardiography showed rat MTAB resulted in significant LV hypertrophy associated with a biphasic change in fractional shortening compared to sham controls. Six weeks after banding, acute measurements of LV pressures and volumes revealed significant changes in systolic and diastolic function associated with decreases in ventricular contractility and compliance. Histology showed increases in fibrosis. Differences in severity of disease between rat strains were observed suggesting MTAB combined with ZFN engineering can reveal functional cardiac effects and supports the role of the Mas1 receptor in cardiac fibrosis.HL082798