The physiological mechanisms underlying leaf growth inhibition under salt stress are not fully understood. Apoplastic pH is considered to play an important role in cell wall loosening and tissue growth and was demonstrated to be altered by several growth-limiting environmental conditions. In this study we have evaluated the possibility that inhibition of maize (Zea mays) leaf elongation by salinity is mediated by changes in growing cell wall acidification capacity. The kinetics of extended apoplast pH changes by leaf tissue of known expansion rates and extent of growth reduction under stress was investigated (in vivo) and was found similar for non-stressed and salt-stressed tissues at all examined apoplast salinity levels (0.1, 5, 10, or 25 mM NaCl). A similar rate of spontaneous acidification for the salt and control treatments was demonstrated also in in situ experiments. Unlike growing cells that acidified the external medium, mature nongrowing cells caused medium alkalinization. The kinetics of pH changes by mature tissue was also unchanged by salt stress. Fusicoccin, an enhancer of plasmalemma H(+)-ATPase activity level, greatly stimulated elongation growth and acidification rate to a similar extent in the control and salt treatments. That the ability of the growing tissue to acidify the apoplast did not change under same salt stress conditions that induced inhibition of tissue elongation rate suggests that salinity does not inhibit cell growth by impairing the acidification process or reducing the inherent capacity for cell wall acidification.