There remains uncertainty shrouding the role of noradrenaline containing (NAergic) neurones in the brainstem for regulating arterial pressure. An earlier study used a neurotoxin – 6-hydroxydopamine (6OHDA) to lesion these neurones and reported lability in mean arterial pressure (MAP) and hypertension [2]. In this study we have examined the role of A2 neurones in regulating arterial pressure in normotensive rats. A lenti viral vector (LV-PRSx8-Kir2.1-IRES-eGFP) was designed to induce expression of an inwardly rectifying potassium channel (Kir2.1) in NAergic neurones to electrically silence them. The PRSx8 promoter in our vector (LV-PRSx8-Kir-IRES-eGFP) is a synthetic promoter of about 260 bp. It encodes the binding sites for Phox2 transcription factor [1]. The binding has been multimerised eight times and attached to a TATA initiation site. Rats were telemetered for chronic blood pressure recordings under ketamine (60 mg kg^-1) and medetomidine (250 μg kg^-1, both I.M.) anaesthetic. Anaesthesia was reversed with a subcutaneous injection of atipamezole (1 mg kg^-1). The virus was injected into the caudal NTS bilaterally (108 ifu ml^-1; 500nl per site; anaesthesia as above). Injection sites were determined from the expression of enhanced green fluorescent protein (eGFP) and Kir2.1 expression validated with real time RT-PCR. Control animals were injected with LV-PRS-eGFP (n=4), with none of the cardiovascular changes associate with LV-PRSx8-Kir-IRES-eGFP. Our data from the normotensive rats indicates that LV-PRSx8-Kir2.1-IRES-EGFP triggers a gradual increase in MAP (from 96.1 ± 2 to 104.1 ± 3 mmHg, mean ± S.E.M., P< 0.05 ANOVA) at 21 days post-injection without a change in spontaneous cardiac baroreflex gain (n=6). Moreover, spectral analysis of systolic blood pressure indicates an increase in the very low frequency from (3.50 ± 0.47 mmHg2 to 4.25 ± 0.45 mmHg2, P< 0.01 ANOVA) indicative of a neurohumoral mechanism. We are presently assessing the role of A2 neurones in the spontaneously hypertensive rats. To date, our findings suggest that A2 neuronal activity in the normotensive rats play a key role in the regulation of arterial pressure.