Background Hypertension is associated with heightened activation of the sympathetic nervous system where a significant component of the over-activity occurs at the end organ. In particular post-ganglionic sympathetic neurones (PGSN) show enhanced intrinsic excitability resulting in greater transmitter release1. Furthermore intracellular Ca2+ transients are significantly enhanced in the SHR stellate neurons compared to age matched neurons from normotensive rats. Interestingly, this Ca2+ phenotype is also seen in the stellate neurons from the pre-hypertensive SHR, suggesting it is an early hallmark of the disease. The increased Ca2+ transients have been shown to be due in part to altered mitochondrial Ca2+ handling2, but this does not explain the total event. In this study we investigated the whole cell Ca2+ current in cardiac sympathetic stellate ganglions of the SHR and WKY in order to elucidate whether the neuronal Ca2+ channels are involved in the neuronal phenotype seen in animals with a pre-disposition to high blood pressure. Methods & Results Cardiac stellate ganglia were excised from 4 week old male pro-hypertensive SHR and WKY rats in accordance with the Home Office Animals (Scientific Procedures) Act 1986 (UK). The ganglia were digested with collagenase (1 mg/ml) and trypsin (2 mg/ml) and mechanically separated to generate a single cell suspension. Whole cell voltage clamp recordings were performed by holding the cell at -90 mV before a set of voltage steps from -60 to +50 mV were applied at 10 mV intervals. Access to the cell was obtained in normal Tyrode solution before the desired current was isolated using a modified Tyrode solution containing 2 mM Ba2+ and 1 µM Tetrodotoxin. Greater than 75% series resistance compensation was applied to all cells and a cellular resting membrane potential of > -40 mV was required for inclusion in the study. Experiments were conducted at 37°C. We show that the whole cell Ca2+ current in the stellate neurons was significantly larger in the SHR (-27.7 ± 1.8 pA/pF; n=7) when compared to the WKY (-22.2 ± 1.3 pA/pF; n=8 p<0.05. Unpaired T-test). Conclusions These data suggest that a part of the abnormally high intracellular Ca2+ levels observed in stellate neurons from the SHR arise from dysregulation of the neuronal Ca2+ channel. This feature is seen at an early stage in the development of the disease itself, and also suggests a neuronal Ca2+ channelopathy is present in this genetic based model of hypertension. Key words: Hypertension, channelopathy, stellate neurons, electrophysiology