Growing evidence suggests that the TWIK-related Acid Sensitive K⁺ (TASK) channels have a functional role in the cardiovascular system. In pulmonary artery (PA), compelling evidence has suggested that TASK-1 is a major contributor to the background K⁺ current that support the membrane potential (E_m) of the smooth muscle cells. However, due to poor selectivity of its modulators, the role of TASK-1 channels in the functional regulation of tone in pulmonary arteries remains elusive. The purpose of this study was to investigate the properties of PA isolated from mice in which the TASK-1 gene has been deleted, compared with their wild type controls (C57BL/6 mice). Intra-PAs (200μm diameter) were isolated from C57BL/6 mice and mice in which the TASK-1 and TASK-3 genes had been deleted (TASK1/3 KO, Aller et al., 2005). TASK-3 is not expressed in PA (Gardener, Johnson et al., 2004). Vessels were mounted on a small vessel myograph for isometric tension measurement. The responses to various drugs were recorded and expressed relative to a reference contraction elicited by application of 50mM KCl at the beginning of each experiment. Statistical analysis was performed using Student’s t-test, with 0.05 as a critical value. Responses of PA to 50mM KCl were not significantly different between C57BL/6 mice (292 ± 54 mN, N=13 vessels) and TASK1/3 KO mice (237 ± 42 mN, N=11). The addition of 10mM KCl, the K⁺ channel modulators 4-AP (1mM) and levcromakalim (10µM), or the L-type calcium channel blocker nifedipine (1µM), did not elicit any significant response in either the TASK1/3 KO (N=6) or C57BL/6 mice (N=6). The contractile response of PA to phenylephrine (PE) had a pEC₅₀ of 6.6 ± 1.3 in C57BL/6 (N=4) and 6.8 ± 1.8 in TASK1/3 KO mice (N=4), with maximum responses (10µM) of 173 ± 37 % and 178 ± 15 %, respectively, of the response to 50mM KCl. For serotonin the pEC₅₀ and maximum responses were, respectively, 6.9 ± 0.3 and 379 ± 94 % in C57BL/6 mice (N=4) and 7.1 ± 0.1 and 267 ± 31 %, respectively, for TASK1/3 KO (N=4). Statistical analysis of both pEC₅₀ and the efficacy of PE and serotonin showed no difference between the TASK1/3 KO and their wild type control. The PA isolated from TASK1/3 KO mice does not display any response to 10mM KCl, K⁺ channel modulators or nifedipine, suggesting that the E_m is not depolarised and that artery is fully dilated as in the C57BL/6 mice. Responses to the agonists PE and serotonin were also unchanged. Further experiments are in progress to investigate other possible effect of TASK-1 deletion, in order to discriminate the contribution of the TASK channels to the overall background K⁺ channels in PA smooth muscle cells. The results thus far do not, however, support a major physiological role for TASK-1 in mouse PA.