The resting potential of pulmonary artery smooth muscle cells (PASMC) is determined by a non-inactivating potassium current (I_KN ). The molecular nature of the voltage-dependent component of this current is yet to be identified. This current has properties consistent with neuronal 'M' current mediated by heteromeric KCNQ2/3 channels. Moreover, recently we found that the blockers of KCNQ channels are potent pulmonary vasoconstrictors. We therefore investigated if KCNQ isoforms are expressed in pulmonary artery smooth muscle and if so whether they contribute to the regulation of the membrane potential. RT-PCR and immunocytochemical analysis showed the presence of KCNQ1, KCNQ3, KCNQ4 and KCNQ5 mRNAs and proteins in rat isolated pulmonary artery and PASMC, respectively. A single band of expected size (99kDa) for KCNQ5 subunit was recognized on western blot. Functional investigation of the expression of the KCNQ channels using whole-cell patch-clamp techniques revealed that linopirdine and XE991 affected the resting K⁺ current and resting potential in PASMC. In current clamp, XE991 (1 mM) and linopirdine (10 mM) depolarised the PASMC by 13.3 ± 1.5 and 14 ± 3 mV, in voltage clamp I_KN was inhibited by 41.2 ± 7 % and 38.2 ± 6.3 %, respectively. These data show that KCNQ channels are expressed in rat PASM and may contribute to the resting membrane conductance.