The regulatory mechanisms for the aluminium (Al)-induced efflux of K(+) and malate from the root apex of Al-resistant wheat ( Triticum aestivum L. cv. Atlas) were characterized. Treatment with 20 mM tetraethylammonium (TEA) chloride, a K(+)-channel inhibitor, blocked the Al-induced K(+) efflux by 65%, but blocked the Al-induced malate efflux only slightly. Lanthanum (La(3+)) or ytterbium (Yb(3+)) strongly inhibited the K(+) efflux, but slightly increased malate efflux. These lanthanides applied together with Al did not affect the Al-induced malate efflux, but reduced the Al-induced K(+) efflux by 57% for La(3+) and by 35% for Yb(3+). By contrast, pretreatment with 50 microM niflumic acid, an anion-channel inhibitor, strongly suppressed the Al-induced malate efflux, but did not affect the Al-induced K(+) efflux. The efflux of K(+) uncoupled with that of malate resulted in the alkalization of intracellular pH in the root apex, suggesting that the release of K(+) coupled with malate plays an important role in stabilizing intracellular pH. Copper (Cu(2+)) induced the release of K(+) via a TEA-insensitive pathway without the release of malate in both Al-resistant and Al-sensitive (cultivar Scout) wheat. Simultaneous application of Al and Cu(2+) to the root apices resulted in TEA-sensitive K(+) efflux in Atlas but not in Scout, suggesting that Al competes with Cu(2+) for K(+) efflux. Taken together, these results suggest that Al-induced K(+) efflux is mediated by both TEA- and lanthanide-sensitive K(+) channels, although this induction is not a prerequisite for the induction of the release of malate.