Vascular smooth muscle cells express several types of potassium (K + ) channels that control physiological functions including contractility, migration, proliferation, and differentiation. Five primary classes of K + channel are present in vascular smooth muscle cells: large-conductance Ca 2+ -activated K + (BK), voltage-dependent K + (K V ), inward-rectifier K + (Kir), adenosine triphosphate (ATP)-sensitive K + (K ATP ), and two-pore domain (tandem pore domain) K + (K2P) channels. Vascular smooth muscle cells can express specific submembers, splice variants, and auxiliary subunits of these five K + channel classes to customize their properties. Expression patterns of K + channels in smooth muscle cells can vary depending on vessel type, size, and anatomical origin. The expression, activity, trafficking, and surface abundance of K + channels can be regulated by a wide variety of stimuli, including membrane voltage, ions, molecules, lipids, and proteins, including those generated by signal transduction pathways. K + channel function can exhibit sexual dimorphism, change in conditions such as pregnancy and aging, and alter in different diseases, including systemic and pulmonary hypertension, diabetes mellitus/metabolic syndrome, and brain disorders. Genetic mutations in genes that encode K + channels are also associated with pathological alterations in vascular smooth muscle function. Here, we provide a comprehensive summary of approximately 40 years of literature investigating the expression, regulation, function, and pathological modification of BK, K V , Kir, K ATP , and K2P channels in vascular smooth muscle cells.