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. The gene discussed is AGT; the disease is cardiac hypertrophy.