Understanding the cause and maintenance of hypertension is critical for generating effective clinical treatments. Vascular tone is controlled by sympathetic nerve activity causing peripheral vasoconstriction. Respiratory-sympathetic coupling is the phenomenon whereby bursts of sympathetic nerve activity are modulated by respiration. In an animal model of essential hypertension the amplitude of sympathetic activity is elevated during the post-inspiratory period, contributing to hypertension (Simms et al. 2009). We do not yet understand the significance of this respiratory-sympathetic bursting pattern and phase vascular tone generation. Thus, we aimed to assess the impact of respiratory modulated bursts of sympathetic activity on vascular resistance (VR). Adult male Wistar rats (n=8) were anaesthetised with 1.2-1.5g/kg urethane and 60mg/kg alpha-chloralose i.p. The left carotid artery was cannulated to record arterial pressure and a flow probe applied to the left femoral artery to record femoral artery flow. Femoral VR was calculated as mean arterial pressure divided by mean vascular flow. The left lumbar sympathetic chain was located and the L4 sympathetic ganglia isolated and a cuff electrode applied for electrical stimulation. The working stimulus voltage was determined as that producing a half-maximal increase in VR (0-2.5V, 2ms pulse width, 40Hz). The nerve was stimulated with two respiratory bursting patterns to model 1Hz and 2Hz respiratory rates. The burst duration matched previous reports of the respiratory-sympathetic burst duration (250ms). Each pattern was compared to tonic stimulation at of the same average spike frequency (2Hz, 4Hz, 8Hz and 10Hz). Values are the maximum change in VR relative to baseline, presented as mean ± S.E.M and compared by Two-way repeated-measures ANOVA. During all stimulation protocols, VR increased maximally at the start of stimulation and then decreased without reaching baseline after 5s of sympathetic nerve. At 1Hz respiratory bursting pattern and 8Hz average spike frequency femoral VR increased (57.8±4.0%) more than matched-tonic nerve stimulation (44.8±4.9%; p<0.01). These results suggest that respiratory modulated bursting maintains a greater VR than tonic sympathetic activity. This could support the results of mathematical modelling of sympathetic innervation of the vasculature (Briant et al., 2015) in which this phenomenon was proposed to be due to decreased clearance of noradrenaline during bursting stimulation. Therefore, the existence of respiratory-sympathetic coupling in addition to elevated sympathetic nerve activity observed in hypertensive patients is likely to exacerbate vasoconstriction.