A moderate increase in extracellular K+ induces relaxation of small arteries via augmenting inwardly rectifying K+ current. The K+-vasodilation is one of the mechanisms for the regional control of blood flow in response to neuronal and skeletal muscle activity. Previously we reported that exercise training (ExT) upregulates Kir current in smooth muscle cells of cerebral and skeletal arteries (CA and DFA). Here we investigated whether Kir current and K+-vasodilation are affected in these arteries of hypertensive rats with or without ExT. To establish hypertension, rats were implanted with osmopumps delivering either Ang II (125 ng/kg/min) or saline. At 4 weeks, smooth muscle cells of CA (CASMCs) and DFA (FASMCs) were isolated and then we voltage clamped to evaluate the Ba2+-sensitive Kir current and voltage-dependent K+ current. The current density of both Kir and Kv (pA/pF) decreased in Ang II-treated hypertensive rats (AII-R). We trained rats with treadmill running for the latter two weeks (3rd and 4th weeks of Ang II application). ExT recovered Kir and Kv currents in CASMCs and FASMCs. At the same time depolarizing inward conductance (nonselective cation current) was also increased by ExT in CASMCs while not in FASMCs. This background inward current was partly inhibited by amiloride, an inhibitor for ENaC and ASIC channel. Also GTPγS, non-hydrolysable GTP analogue, induced a slowly inward current in AII-R CASMCs. And this GTPγS-activated current was further increased by ExT. The K+-vasodilation was monitored by using video-analysis of pressurized artery. Consistent with the changes in Kir current, vasodilation by adding 2 mM KCl was weakened in both DFA and CA from AII-R. The K+-vasodilation of DFA but not of CA was recovered in AII-R with ExT. A bath application of Ang II did not induce constriction of CAs, suggesting that the changes in K+ channels are not directly induced by Ang II but by indirect effects of hypertension. The decreased K+ conductance might reflect an adaptive change of resistance arteries to prevent over-perfusion of vital organs such as brain. The recovery of Kir and Kv currents by ExT might be one of the mechanisms for the beneficial effects of regular exercise on hypertension.