The intrinsic properties of sympathetic preganglionic neurones (SPNs) are important in determining the output characteristics of the sympathetic nervous system. The potassium A-current (IA) is prominent in SPNs, and in other systems has been shown to regulate firing frequency and after-hyperpolarisation (AHP) shape [1]. Sympathetic vasomotor discharge is known to be bursty, and one rhythm is entrained to the central respiratory pattern generator output. We have shown that in spontaneously hypertensive rats (SHRs) there is an increase in the amplitude of respiratory-sympathetic coupling [2] and hypothesise that this may be due to changes in IA. To test this hypothesis we have built a NEURON [3] model. By fitting our A-current parameters to detailed experimental data [4], the model exhibited physiological responses similar to those of SPN in vivo, and steady-state curves that well-fit data for the normotensive Wistar (WKY) rat. Features of the IA that could provide a SHR response were investigated; one particular parameter, maximal conductance density gKA, was identified as being capable of turning the WKY cellular response profile into that seen in SHR with increased excitability [5]. To better understand the effect of altered gKA on cell excitability we first examined action potential morphology and found small, biologically minor, changes in threshold (-0.24mV) spike amplitude (+0.24mV) and half-width (+0.2ms) for the SHR strain. The AHP amplitude (WKY=9.87mV vs SHR=5.23mV) was markedly reduced in the SHR (but not duration). We next generated a frequency-modulated synaptic input into our SPN to mimic the effect of a respiratory entrained drive, with inter-event intervals (IEI) between 980ms and 20ms, and quantified the influence of gKA on the output characteristic. Within bursts, the proportion of successfully transmitted EPSPs significantly decreased in the WKY (SHR=0.99±0.01, WKY=0.6±0.1, p<0.001) and it was noted that the higher frequency component was specifically attenuated. Examination of EPSP shape (1HZ stimulation) showed that increasing IA shortened EPSP duration (τSHR=28ms,τWKY=13ms) with little effect on amplitude (decreased by <3%). This change in EPSP decay had a major effect on EPSP summation at higher frequencies in the Wistar model (IEI<60ms; 2.5-fold decrease in EPSP amplitude gain; SHR=4.3±0.1mV, WKY=1.2±0.8mV) which, when combined with the augmentation in AHP amplitude, acts to low-pass filter the sympathetic output. Our data shows that a reduction of gKA in SHRs would result in a reduced filtering of respiratory-modulated (and indeed any high frequency) input, and therefore an amplification of respiratory-sympathetic coupling. These modelling data are consistent with IA playing a major role in determining SPN excitability as a tuneable low pass filter, thus regulating sympathetic output.