In the structurally normal heart, ventricular tachycardia (VT) frequently arises from the right ventricular outflow tract (RVOT). It has been postulated that this is due to triggered activity. We have investigated the molecular phenotype of the RVOT to determine if this could account for its arrhythmogenicity. Wistar rats (3-months old) were sacrificed according to a Home Office-approved method. Tissue samples for qPCR were taken from the right ventricular apex (RV) the infundibulum (RVOT1) and ventriculo-arterial junction (RVOT2) of the RVOT (n=8). qPCR was performed using TaqMan low density array cards. In total, 96 transcription factors, ion channels, extracellular matrix genes and signalling molecules were analysed. The abundance of transcripts was normalised to 4 different reference genes (18S, αMYH6, NCX1 and the average abundance of 90 transcripts). The results were qualitatively similar using all methods. Statminer software (Integromics) was used to determine significant differences in relative abundance. In addition, intracellular action potential recordings were made using 20-30 MΩ, 3M KCl-filled microelectrodes from the endocardial surface of an open-book preparation of the RVOT (n=3 animals); only data from 1 preparation are presented. Compared to the RV, expression of Tbx3, was significantly increased by ~70% in the RVOT. Expression of Nav1.5, was significantly reduced by ~50% in the RVOT (compared to the RV) and this is expected to result in an action potential with a lower maximum rate of rise (dV/dtmax) and smaller amplitude. Expression of Kir2.1 and Kir2.2, was significantly reduced by ~34% and ~10%, respectively, in the RVOT and this is expected to result in a more positive maximum diastolic potential. Other differences are: for example, Kv1.5 and KChiP2 were significantly increased by 68% and 98%, and Kir3.1, Kir3.4, RYR2 and NCX1 were significantly reduced by 55%, 50%, 34% and 32%, in the RVOT (compared to the RV). Recordings of intracellular action potentials were made from 6 RV, 3 RVOT1 and 7 RVOT2 sites (in one preparation). Electrical stimuli of twice threshold strength, 2 ms duration and at 1 Hz evoked action potentials with a maximum rate of rise (dV/dtmax) of 360±18, 299±19 and 210±36 V/s in the RV, RVOT1 and RVOT2 regions, respectively. Corresponding action potential amplitudes were 105±2, 101±3 and 86±2 mV. The maximum diastolic potential was 77.3±1.1, -75.1±2.8 and 74.6±2.2 mV in the RV, RVOT1 and RVOT2 regions, respectively. The RVOT exhibits various characteristics similar to those of the sinoatrial and atrioventricular nodes. It is known that the RVOT shares the same embryonic origin from ‘primary myocardium’ as the sinoatrial and atrioventricular nodes and this is likely to be the reason for nodal-like myocytes in the RVOT. This offers a plausible explanation for the arrhythmia burden of the RVOT.