Background. The potassium channel blocker tetraethylammonium blocks the flowinduced increase in endothelial intercellular adhesion molecule-1 (ICAM-1). We have investigated the subtype of potassium channel that modulates flow-induced increased expression of ICAM-1 on saphenous vein endothelium. Methods. Cultured human saphenous vein endothelial cells (HSVECs) or intact saphenous vein were perfused, at fixed low and high flows, in a laminar shear chamber or flow rig respectively, in the presence or absence of potassium channel blockers. Expression of K⁺ channels and endothelial ICAM-1 was measured by real-time polymerase chain reaction and/or immunoassays. Results. In HSVEC the application of 0.8N/m² (8 dynes/cm²) shear stress resulted in a 2-4 fold increase in cellular ICAM-1 within 6h, p<0.001. In intact vein a similar shear stress, with pulsatile arterial pressure resulted in a 2-fold increase in endothelial ICAM-1/CD31 staining area within 1.5h, p<0.001. Both increases in ICAM-1 were blocked by inclusion of 100nM apamin in the vein perfusate, whereas other K⁺ channel blockers were less effective. Two subtypes of small conductance calcium-activated K⁺ channel (selectively blocked by apamin), were expressed in HSVECs and vein endothelium, SK3>SK2. Conclusions. Apamin blocked the upregulation of ICAM-1 on saphenous vein endothelium in response to increased flow, to implicate small conductance calcium activated K⁺ channels in shear stress/flow mediated signalling pathways.