Inhibition of leaf growth by salt stress is a complex mechanism and has been proposed to be controlled by root-sourced ABA signals. In the current study two maize (Zea mays L.) genotypes differing in salt resistance were compared for leaf cell wall acidification and their relationship with leaf growth under ABA and salt stress. The decrease in cell-wall acidification due to lower plasma membrane (PM) H⁺-ATPase proton pumping during the first phase of salt stress was a major cause of reduction in leaf expansion of salt-sensitive Pioneer 3906. The results reported in this study provide evidence that the partial inhibition of PM H⁺-ATPase proton pumping in leaves of Pioneer 3906 under salt stress involves ABA signalling, which down-regulates the transcription of the MHA3 isoform of H⁺-ATPase. The data indicate that MHA3 is an efficient isoform of H⁺-ATPase with higher H⁺/ATP coupling ratio. Unchanged levels of enzyme concentration in the membranes of the ABA and salt-treated plants show that the ABA-induced down-regulation of MHA3 is compensated with the up-regulation of an unknown inefficient isoform. In contrast, H⁺-ATPase proton pumping and cell-wall acidification remained unaffected in leaves of the salt-resistant genotype SR 03 during the first phase of salt stress. A differential response of MHA3 transcription to ABA reduced the sensitivity of SR 03 to ABA-induced inhibition of leaf growth and therefore contributed to the salt resistance of SR 03.