The apoplastic pH of intact green leaves of Bromus erectus was measured non-invasively by inserting blunt microelectrodes through stomatal openings. After making electrical contact, the recorded signal was stable for hours, yielding a pH of 4.67p0.10. The leaves responded to ' light-off ' with an initial transient acidification and subsequent sustained alkalinization of 0.2-0.3 pH ; ' light-on ' caused the opposite response. Flushing the leaves with 280 nmol NH $ mol −" air within 18p6 s alkalinized the apoplast by 0.22p0.07 pH, followed by a slower pH increase to reach a steady-state alkalinization of 0.53p0.14 after 19p7 min. This pH shift was persistent as long as the NH $ was flushed, and readily returned to its initial value after replacing the NH $ with clean air. The resultant [NH % + ] increase within the apoplast was measured with a NH % + -selective microelectrode. In the presence of 280 nmol NH $ mol −" air, apoplastic NH % + initially increased within 15p10 s to 1.53p0.41 mM, to reach a steady state of 1.62p0.16 mM after 27p7 min. An apoplastic buffer capacity of 6 mM pH −" unit was calculated from the initial changes of pH and [NH % + ], whereas the steady-state values yielded 2.7 mM pH −" . Infiltrated leaves responded to NH % + with concentration-dependent depolarizations, the maxima of which yielded saturation kinetics indicating carrier-mediated NH % + uptake into adjacent cells, as well as a linear component indicating nonspecific transport. We infer that the initial alkalinization is due to rapid conversion of NH $ to NH % + , whereas the slower pH increase would be caused by regulatory processes involving both membrane transport, and (mainly) NH % + assimilation. Possible consequences of the NH $ -induced pH shift for the development of plants growing in polluted areas are discussed.