Plants can survive in soils of low micromolar potassium (K) concentrations. Root K intake is accomplished by the K channel AKT1 and KUP/HAK/KT type high-affinity K transporters. Arabidopsis HAK5 mutants impaired in low K acquisition have been identified already more than two decades ago, the molecular mechanism, however, is still a matter of debate also because of lack of direct measurements of HAK5-mediated K currents. When we expressed AtHAK5 in Xenopus oocytes together with CBL1/CIPK23, no inward currents were elicited in sufficient K media. Under low K and inward-directed proton motive force (PMF), the inward K current increased indicating that HAK5 energetically couples the uphill transport of K to the downhill flux of H. At extracellular K concentrations above 25 μM, the initial rise in current was followed by a concentration-graded inactivation. When we replaced Tyr450 in AtHAK5 to Ala the K affinity strongly decreased, indicating that AtHAK5 position Y450 holds a key for K sensing and transport. When the soil K concentration drops toward the range that thermodynamically cannot be covered by AKT1, the AtHAK5 K/H symporter progressively takes over K nutrition. Therefore, optimizing K use efficiency of crops, HAK5 could be key for low K tolerant agriculture.