Abnormalities in conduction velocity (CV) can lead to the generation of re-entrant arrhythmias, a common precursor of ventricular fibrillation (VF). CV is determined by intercellular gap-junction resistance and is thought to be increased during B-adrenergic stimulation although the mechanism is poorly understood. Studies suggest that increasing intracellular cAMP levels increases gap-junction conductance but effect on CV in intact heart is unclear. Adult male Wistar rats (300-500g) were euthanised and hearts Langendorff perfused with modified Tyrode’s solution. CV was recorded using custom electrodes, consisting of bipolar stimulating electrodes and two sets of bipolar recording electrodes. Channel 1 (Ch1) recording electrodes were positioned 1mm from Channel 2 (Ch2) recording electrodes. These electrodes were placed on the epicardial surface of the left ventricle and rotated to achieve record on the axis of maximal CV. The ventricle was paced continuously at 7HZ and the delay between the AP wavefront reaching Ch1 and Ch2 was recorded at a sampling rate of 10 KHz. From this CV could be calculated. In some experiments, blebbistatin (3-10μM ) was perfused onto the heart 25 mins before experimental measurements to minimise movement artefacts in CV measurements. Drugs which raise intracellular cAMP were applied for 5 mins and continuous recordings of CV were made prior to during and on washout. Under control conditions the average CV was 66.3±5 cm.s-1 .The phosphodiesterase (PDE) inhibitor, 3-isobutyl-1-mthylxanthine (IBMX 100μM) significantly increased CV by 9.7%±1.3 (p< 0.001 n=4) compared to DMSO control group. Isoproterenol (Iso, 100nM) significantly increased conduction velocity by 9.0%±1.4 (p<0.01 n=4). The time course of the CV response to IBMX was significantly slower than the chronotropic response (p<0.05 n=4), with a half time of 58.7±9.1s for the chronotropic response and a half time of 133.1±20.2s for the CV response. Similar difference in chronotropic and dromotropic responses were also seen in response to iso. These results suggest that β-adrenergic stimulation may increase ventricular CV via a stimulatory G-protein mediated pathway. Whether it is via activation of protein kinase A (PKA) or exchange protein directly activated by cAMP (EPAC) has yet to be established. If the phase lag between chrontropic and dromotropic responses applies during increased cardiac sympathetic activity it may generate a period where conduction block and re-entry may be more common.