Heart　failure　(HF)　is　a　serious　cardiovascular　disease　and　is　characterized　by　exaggerated　sympathetic　activity.　In　this　paper,　we　review　these　limited　studies,　with　particular　emphasis　on　examining　the　role　of　the　paraventricular　nucleus　(PVN)　in　the　neurohumoral　excitation　in　HF.　The　PVN　is　an　important　neuroendocrine　and　preautonomic　output　nucleus,　and　is　considered　as　the　important　central　site　for　integration　of　sympathetic　nerve　activity.　Accumulating　evidences　demonstrate　that　a　number　of　neurohumoral　processes　are　involved　in　the　pathophysiology　of　HF,　such　as　renin-angiotensin　system　(RAS),　proinflammatory　cytokines　(PICs),　neurotransmitters,　and　reactive　oxygen　species　(ROS).　Recent　studies　about　neurohumoral　regulation　indicate　that　angiotensin　II　type1　receptor　(AT1-R)　is　the　important　product　mediated　by　cytoplasmic　nuclear　factor-kappa　B　(NF-κB)　which　is　up-regulated　along　with　elevated　PICs　and　angiotensin　II　(ANG　II)　in　the　PVN　of　HF　rats.　These　findings　suggest　that　the　NF-κB　mediates　the　cross-talk　between　RAS　and　PICs　in　the　PVN　in　HF.　The　further　studies　indicate　that　the　interaction　between　AT1-R　and　NF-κB　in　the　PVN　contributes　to　oxidative　stress　and　sympathoexcitation　by　modulating　neurotransmitters　in　heart　failure,　and　the　superoxide　activates　NF-κB　in　the　PVN　and　contributes　to　neurohumoral　excitation.　In　conclusion,　the　neurohumoral　excitation　in　HF　is　based　on　the　interaction　of　RAS,　PICs,　ROS,　NF-κB　and　neurotransmitters　in　the　PVN;　and　the　activated　NF-κB　in　the　PVN　modulates　the　neurotransmitters　and　contributes　to　sympathoexcitation　in　rats　with　heart　failure.