Our major observations were that OT accelerated AngII-induced hypertension in a dose dependent manner leading to a compensatory phase of cardiac hypertrophy with increased heart weight and left ventricular mass; but without significant changes in collagen deposition and myocardial fibrosis, or function as determined by evaluation of the left ventricular ejection fraction and fractional shortening. Here, AGT is linked to Myocardial fibrosis.