In heart failure, it has been recognized that the sympathetic nervous system (SNS) is activated and the imbalance of the activity of the SNS and vagal activity interaction occurs. The abnormal activation of the SNS leads to further worsening of heart failure. Many previous clinical and basic studies have demonstrated that the abnormal activation of the SNS is caused by the enhancement of excitatory inputs including changes in: (1) peripheral baroreceptor and chemoreceptor reflexes; (2) chemical mediators that control sympathetic outflow; and (3) central sites that integrate sympathetic outflow. In particular, the abnormalities in central SNS regulation due to the renin angiotensin system-oxidative stress axis have recently been in focus. In the treatment of heart failure, the inhibition of the activated SNS, such as with beta-blockers and/or exercise training, is important. Furthermore, many experimental studies have demonstrated that vagal stimulation has beneficial effects on heart failure, and recently several clinical studies have also demonstrated that vagal stimulation is a possible novel therapy for heart failure. In conclusion, we must recognize that heart failure is a complex syndrome with an autonomic nervous system dysfunction, and that the autonomic imbalance with the activation of the SNS and the reduction of vagal activity should be treated.
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