Vascular smooth muscle (VSM) cells and endothelial cells (EC) that form the walls of arterioles express a diverse array of ion channels that play important roles in the function of these cells and the microcirculation in both health and disease. Potassium channels, in particular, importantly regulate the function of these cells primarily through their impact on membrane potential. In cells that possess voltage-gated calcium channels (VGCC) such as VSM and perhaps some EC, membrane potential importantly controls the open state probability of the VGCC, which determines intracellular calcium and hence the function of these cells. Membrane potential also importantly impacts the electrochemical gradient for diffusion of calcium into cells through non-voltage gated channels such as those in the transient receptor potential family of ion channels. Finally, membrane potential, through its ability to be transmitted between cells through gap junctions, also acts as an important signal for cell-cell communication in the arteriolar wall. Microvascular VSM cells express at least four different classes of potassium channels including inward-rectifier potassium channels (KIR), ATP-sensitive potassium channels (KATP), voltage-gated potassium channels (KV) and large conductance calcium-activated potassium channels (BKCa). VSM KIR participate in dilation induced by elevated extracellular potassium and may also be activated by C-type natriuretic peptide, a putative endothelium-derived hyperpolarizing factor (EDHF). Vasodilators acting through cAMP or cGMP signalling pathways in VSM may open KIR, KATP, KV and BKCa causing membrane hyperpolarization and vasodilatation. VSM BKCa also may be activated by epoxides of arachidonic acid (EETs) identified as EDHF in some systems. Conversely, vasoconstrictors may close KATP, KV and BKCa through protein kinase C, Rho-kinase or c-Src pathways and contribute to VSM depolarization and vasoconstriction. Despite the inhibitory effects of these signaling pathways on KV and BKCa, the net depolarization, and in the case of BKCa, the increase in intracellular calcium caused by vasoconstrictors activate both KV and BKCa channels which act in a negative feedback manner to limit the vasoconstrictor-induced depolarization and increase in VSM intracellular calcium and hence prevent vasospasm. While calcium transients through ryanodine receptors (calcium sparks) control BKCa channel function in some smooth muscles, calcium entry through VGCC appears to play a more important physiological role in controlling BKCa function in some microvascular VSM. Microvascular EC express at least five classes of potassium channels including small (sKCa) and intermediate (IKCa) conductance calcium-activated potassium channels, KIR, KATP and KV. Both sK and IK are opened by endothelium-dependent vasodilators that increase EC intracellular calcium to cause membrane hyperpolarization that may be conducted through myoendothelial gap junctions to hyperpolarize and relax arteriolar VSM. Endothelial KIR serve to amplify sKCa- and IKCa-induced hyperpolarization and allow active transmission of hyperpolarization along EC through gap junctions. Endothelial KIR channels also may be opened by elevated extracellular potassium and participate in potassium-induced vasodilatation. Endothelial KATP channels may be activated by vasodilators as in VSM and EC KV channels may provide a negative feedback mechanism to limit depolarization in some endothelial cells. Thus, potassium channels play a central role in the regulation of many aspects of microvascular cell function.