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目的 To explore the effects and mechanisms of vasopressin involved in asthma induced by psycological stress in mice.方法 The mice of 6-8 weeks old mice were divided into three groups(n= 8)：Control,Asthma,Asthma+psychological stress(PS).Here,marked asthma exacerbations were noted owing to significantly elevated levels of vasopressin(VP)in the cerebrospinal fluid(CSF)and vasopressin receptor(VP-R)in airway-related vagal preganglionic neurons(AVPNs)after psychological stress induction as compared to OVA alone(asthma group).In each group,airway vagal preganglionic neurons were labeled from tracheal wall.VP-R antagonists(SR-49095 or SR-121463A),KT-5720(PKA inhibitor)and Go-7874(PKC inhibitor)were administered by intracerebroventricular(i.c.v.)injection.The involved mechanisms of VP and VP-R were investigated.结果 VP-R antagonists(SR-49095 or SR-121463A)dramatically lowered higher protein levels of PKAα and PKCα induced by psychological stress as compared to OVA alone.KT-5720(PKA inhibitor)and Go-7874(PKC inhibitor)directly revealed the involvement of PKA/PKC in psychological stress asthma.In addition,some notable changes were noted after employing PKA and PKC inhibitors in psychological stress asthma,including reduced asthmatic inflammation(revealed by lower eosinophil peroxidase(EPO)activity,myeloperoxidase(MPO)activity,immunoglobulin E(IgE)level,and histamine release),substantial decrements in inflammatory cell counts(eosinophils and lymphocytes),and decreased cytokine secretion(IL-6,IL-10,and IFN-γ),indicating the involvement of PKA/PKC in asthma exacerbations induced by psychological stress.结论 VP induced psychological stress-induced asthma exacerbations in mice via PKA/PKC signal pathway in AVPNs.