Essential hypertension involves a gradual and sustained increase in total peripheral resistance, reflecting an increased vascular tone. This increased vascular tone is associated with a depolarization of vascular smooth muscle cells (VSMCs) and relies on a change in the expression profile of voltage-dependent ion channels (mainly Ca²⁺ and K⁺ channels) that promotes arterial contraction. Voltage-dependent K⁺ channels (Kv channels) are principal contributors to determine the resting membrane potential of VSMCs. However, the changes in their expression and/or modulation during hypertension are poorly defined, mainly due to their large molecular diversity and to the variations in their expression in the different vascular beds. Here we have undertaken the study of the molecular and functional characterization of Kv channels in VSMCs (both at the mRNA and protein level) and their regulation in essential hypertension by using VSMCs from resistance (mesenteric) or conduit (aortic) arteries obtained from a hypertensive inbred mice strain, BPH, and the corresponding normotensive strain, BPN. Mice were killed by decapitation after isofluorane anaesthesia and arteries were cleaned of connective and endothelial tissues. Real-time PCR using low-density taqman^® arrays reveals a differential distribution of Kv channel subunits mRNA in the different vascular beds as well as arterial bed-specific changes under hypertensive conditions. In resistance arteries, the hypertensive phenotype associates with an increase in the expression of Kcng3 and a decrease in Kcnd1 mRNA. To study the functional relevance of these changes, we characterize the electrophysiological properties of freshly dissociated VSMCs from BPN and BPH mice by using the patch-clamp technique. VSMCs from BPH mesenteric arteries were more depolarized than BPN ones, and showed significantly larger capacitance values (23.43±2.1 versus 13.46± 0.8 pF respectively). We found that Kv channels current density was significantly reduced in BPH mesenteric VSMCs at all voltages. Application of 50 nM stromatoxin inhibited 34% of the Kv current at +40 mV in BPN cells, but only 21% in BPH cells, suggesting that the reduction in the functional expression of Kv2 channels in BPH cells contributes to the decreased Kv current in these cells. These data indicate that impaired Kv2 channel activity, mediated by changes in the expression level of the accessory gamma subunit Kcng3, could contribute to the changes in excitability of VSMCs from resistance arteries during essential hypertenison.