Diabetes increases the risk of developing congestive heart failure, even in the absence of coronary heart disease or hypertension. A growing body of experimental and clinical evidence is accumulating to show diabetes-related cardiac dysfunction (1). The molecular and pathophysiological mechanisms that are responsible for cardiac dysfunction in diabetes include impaired calcium homeostasis, upregulated renin-angiotensin system, increased oxidative stress, altered myocardial substrate and energy metabolism, and mitochondrial dysfunction (1). Dysfunction of the autonomic nervous system is one of the common and serious complications of diabetes, which also can be the major mechanism implicated in the pathogenesis leading to the manifestation of impaired cardiac function in diabetes. Autonomic dysfunction in diabetes impairs exercise tolerance, reduces response in heart rate and blood pressure, and blunts increases in cardiac output in response to exercise (2). In a rat model of streptozotocin (STZ)-induced type 1 diabetes, the impaired release of norepinephrine from cardiac sympathetic nerves in response to electrical field stimulation has been demonstrated (3), indicating reduced cardiac sympathetic nerve activity. An earlier report showed increases in turnover, uptake, and synthesis of norepinephrine in STZ-induced diabetic hearts (4), but this observation does not reach general agreement according to later reports (3,5,6). Whatever changes in norepinephrine stored in cardiac sympathetic nerve terminals, the fall in overflow of norepinephrine produced by cardiac electrical stimulation (3) would reflect an impairment of the presynaptic functional process for releasing norepinephrine from sympathetic nerve endings in hearts from STZ-induced diabetic rats (Fig. 1). Interestingly, the lack of ability of atropine or yohimbine to enhance the norepinephrine release from cardiac sympathetic nerves in STZ rats …