The present new and novel finding is that increased circulating angiotensin II at similar level of myocardial infarction could directory affect brain and cause excessive sympathoexcitation in normal rats without various mechanisms of sympathoexcitation (hemodynamic and cardiopulmonary reflex, baroreflex failure, and/or excess excitation of brain renin-angiotensin system). The gene discussed is AGT; the disease is myocardial infarction.