The sympathetic nervous system plays a role during chronic inflammation. Since levels of nerve growth factor (NGF) are high in inflamed tissues and, in sensory neurons, NGF controls nociception by regulating neuronal sensitivity to noxious stimuli, we hypothesize that NGF also sensitizes sympathetic neurons to bradykinin (BK), a proinflammatory peptide. We cultured rat superior cervical ganglion (SCG) neurons in the presence or absence of NGF. To assess the response of SCG neurons to Bk, we measured cytoplasmic Ca2+ elevations induced by an acute application of Bk. We found Ca2+ elevation to be increased 3-fold in the presence of NGF. These Ca2+ elevations in the presence of NGF depended on external Ca2+ and depolarization of the plasma membrane. Next, we assessed the effect of Bk on the membrane potential by electrophysiological recordings. NGF-treated neurons were significantly depolarized after Bk application, while neurons cultured in the absence of NGF showed no change in membrane potential with Bk. How does NGF render SCG neurons more responsive to a Bk stimulus? We first tested whether NGF application alters BK-induced M current inhibition. Interestingly, we observed full inhibition of M current upon application of BK with and without culture in NGF. Next, we asked whether incubation of SCG neurons with NGF alters activity of other ion channels. One of the ion channels tested, KCa1.1 (Maxi K+ channel), was reduced in current density by 50% in neurons cultured in the presence of NGF. In addition, inhibition of KCa1.1 channels with iberiotoxin in SCG neurons cultured in the absence of NGF depolarized the plasma membrane potential after Bk application. In conclusion, NGF increased Bk-induced electrical excitability of rat SCG neurons by reducing a repolarizing current mediated by KCa1.1 channels. Supported by NIH grant NS008174.