The sympathetic pregangionic neurone (SPN) is the last central site for integration of sympathetic efferent traffic. As such, the integrative properties are of paramount importance in determining the nature of its output. Intracellular recording studies in vitro and in vivo have provided information about the integrative characteristics of the SPN, although this information has never been used to model the integrative properties of the SPN. We have speculated that changes in excitability of SPN may underpin the increase in sympathetic traffic seen in models of hypertension [1,2] and specifically that an alteration in the A-type potassium current (IA) in these neurons may contribute to this change in excitability. Therefore we have built a NEURON model [3] of the SPN including the following features: medial and lateral dendrites, an axon with Hodgkin-Huxley dynamics, and a soma with membrane conductances such as calcium-activated potassium, N- and L-type calcium and potassium afterhyperpolarisation. We used this model to investigate the role of transient rectifier IA in regulating the excitability of SPN. We tailored a Borg-Graham model of IA to match the known dynamic characteristics of experimentally recorded data in rat SPN. Besides alterations of the activation and inactivation parameters and kinetics this also required that the Borg-Graham model of IA be adjusted to allow independent control of the steady-state functions and dynamic time-constants of this current. In silico experiments showed that this refined IA model gave responses similar to those recorded in vitro (see Figure) [4]. Further simulation showed that IA plays an important role in regulating the excitability of SPN and is active at membrane potentials close to rest. Thus, small alterations in the kinetics or density of IA profoundly influence the excitability of SPN with the following features; a reduction in firing frequency in response to an injected current, an alteration in spike accommodation and an alteration in the amplitude and duration of the afterhyperpolarisation. Along with these findings (which are based on preliminary simulations), we found that the output response of SPN to incoming synaptic traffic is dependent on the characteristics of IA. These modelling data are consistent with IA playing a central role in determining SPN excitability and its response to synaptic input, and indicate that changes in its properties could play an important role in elevating the sympathetic nervous system output in hypertensive rats.