Voltage-dependent potassium channels are crucial determinants of smooth muscle membrane potential and ipso facto vascular contractility. Recent work by the authors revealed that Kv7 channels encoded by KCNQ genes influenced vascular reactivity in mouse portal vein (Ohya et al., 2003; Yeung & Greenwood, 2005). The aim of the present study was to ascertain whether KCNQ genes were expressed in rodent cerebral vasculature and to determine if the expression products influenced vascular reactivity. Total RNA was extracted from SD rat and BALB/c mouse basilar arteries (rBA / mBA) and rat middle cerebral arteries (MCA) using the RNeasy mini spin columns (Qiagen, UK) and following DNase I treatment was reverse-transcribed to cDNA using M-MLV (Invitrogen, UK). KCNQ gene expression products were detected using primers specific for the 5 different isoforms. RNA derived from mouse heart and brain was used as positive controls. Isometric tension experiments were performed using segments of rat basilar artery mounted on a wire myograph and bathed in Krebs’ solution aerated with 95%O2 / 5 % CO2 at 37oC. KCNQ1 and KCNQ4 were expressed in the basilar arteries and MCA at sufficiently high levels to be detected easily after 35 PCR cycles (n=3 each). Nested PCR was employed to explore the expression of the isoforms further. Whilst this technique revealed some KCNQ2 to be present KCNQ3 and KCNQ5 were not detected. Appropriate amplicons were detected in the brain and heart samples. In the functional studies, the selective Kv7 channel blocker XE991 (10 µM) contracted rBA from baseline tension to 4.93 ± 0.69 mN in 14 of 15 preparations from 8 animals. This equated to 103 ± 31 % of the contraction produced by 60 mM KCl. The Kv7 channel activator flupirtine (1 and 10 µM) relaxed contractions produced by 1 µM 5HT with a mean relaxation of 72 ± 10 % (n=7 from 4 animals) at 10 µM. These were reversed completely by 10 µM XE991. These studies show that cerebral arteries express KCNQ1 and KCNQ4 prominently and modulation of the ion channels alters markedly cerebral artery basal or 5-HT-induced tone. As flupirtine does not activate Kv7.1 channels these data combined suggest that ion channels encoded by KCNQ4 are important determinants of cerebral blood flow.