High soil salinity constitutes a major environmental constraint to crop production worldwide, and the identification of genetic determinants of plant salt tolerance is awaited by breeders. While the leaf K + to Na + homeostasis is considered as key parameter of plant salt tolerance, the underlying mechanisms are not fully identified. Especially, the contribution of K + channels to this homeostasis has been scarcely examined. Here, we show, using a reverse genetics approach, that the outwardly-rectifying K + channel OsK5.2, involved in K + translocation to the shoot and K + release by guard cells for stomatal closure, is a strong determinant of rice salt tolerance. Upon saline treatment, OsK5.2 function in xylem sap K + load was maintained, and even transiently increased, in roots. OsK5.2 selectively handled K + in roots and was not involved in xylem sap Na + load. In shoots, OsK5.2 expression was up-regulated from the onset of the saline treatment, enabling fast reduction of stomatal aperture, decreased transpirational water flow and therefore decreased transplant Na + flux and reduced leaf Na + accumulation. Thus, the OsK5.2 functions allowed shoot K + nutrition while minimizing arrival of Na + , and appeared highly beneficial to the leaf K + to Na + homeostasis, the avoidance of salt toxicity and plant growth maintaining.