ABSTRACTThe roles of K+uptake and loss in the salinity response of the wild type and the salt‐tolerant mutantstl2ofCeratopteris richardiiwere studied by measuring Rb+influx and loss and the effects of Na+, Mg2+, Ca2+and K+‐transport inhibitors. In addition, electrophysiological responses were measured for both K+and Rb+and for the effects of Na+and NH4+on subsequent K+‐induced depolarizations.stl2had a 26–40% higher uptake rate for Rb+than the wild type at 0.5–10 mol m−3RbCl. Similarly, membrane depolarizations induced by both RbCl and KCl were consistently greater instl2. In the presence of 0–180 mol m−3NaCl,stl2maintained a consistently greater Rb+influx than the wild type.stl2retained a greater capacity for subsequent KCl‐induced depolarization following exposure to NaCl. Five mol m−3Mg2+decreased Rb+uptake instl2; however, additional Mg2+up to 40 mol m−3did not affect Rb+uptake further. Ca2+supplementation resulted in a very minor decrease of Rb+uptake that was similar in the two genotypes. Tetraethylammonium chloride and CsCl gave similar inhibition of Rb+uptake in both genotypes, but NH4Cl gave substantially greater inhibition in the wild type than instl2. NH4Cl resulted in a greater membrane depolarization in the wild type and the capacity for subsequent depolarization by KCl was markedly reduced.stl2exhibited a higher Independent loss of Rb+than the wild type, but, in the absence of external K+, loss of Rb+was equivalent in the two genotypes. Since constitutive K+contents are nearly identical, we conclude that high K+influx and loss exact a metabolic cost that is reflected in the inhibition of gametophytic growth. Growth inhibition can be alleviated by reduced supplemental K+or by treatments that slightly reduce K+influx, such as moderate concentrations of Na+or Mg2+. We propose that high throughput of K+allows maintenance of cytosolic K+under salt stress and that a high uptake rate for K+results in a reduced capacity for the entrance and accumulation of alternative cations such