To assess our hypothesis, we considered that the known various mechanisms of sympathoexcitation in myocardial infarction-induced heart failure should be excluded, and that we increased circulating angiotensin II by subcutaneous infusion in normal rats, not heart failure model rats, without the known various mechanisms of sympathoexcitation in myocardial infarction-induced heart failure. Here, AGT is linked to myocardial infarction.