Activation of potassium channels in vascular smooth muscle (VSM) can oppose vasoconstriction and cause vasodilation of arteries. Vasoconstrictor stimuli such as an elevation of intravascular pressure cause membrane depolarization and an elevation of intracellular calcium which in turn activate large conductance, voltage-dependent and calcium-sensitive potassium (BK) channels and voltage-dependence potassium (Kv) channels to oppose vasoconstriction. Strong inward rectifier potassium (Kir) channels in contrast are activated by membrane hyperpolarization and small elevations of external potassium (3-15 mM). These potassium channel types have unique roles in (parenchymal) arterioles within the brain. Parenchymal arterioles are encased by astrocytic processes ("endfeet"), which translate neuronal activity into calcium signals to modulate arteriolar diameter, and hence blood flow ("neurovascular coupling"). Inhibition of Kv, but not BK channels, causes profound vasoconstriction, a response which is modulated by extracellular glucose (Straub et al. Am J Physiol, 2009). Kir channels in VSM cells of parenchymal arterioles appear to be activated by locally released potassium from the astrocytic endfeet to mediate part of the neuronally evoked dilation (Filosa et al., Nature Neuroscience, 2006. Girouard et al., PNAS, 2010). These results indicate that Kv and Kir channels in the VSM of parenchymal arterioles have important roles in the modulation of blood flow within the brain, including neurovascular coupling.