K analysis of sodium-induced potassium efflux in barley: mechanism and relevance to salt tolerance

• Published in: The New phytologist Vol. 186; no. 2; pp. 373 - 384
• Main Authors: Britto, Dev T, Ebrahimi-Ardebili, Sasha, Hamam, Ahmed M, Coskun, Devrim, Kronzucker, Herbert J
• Format: Journal Article
• Language: English
• Published: Oxford, UK : Blackwell Publishing Ltd 01.04.2010; Blackwell Publishing
• Subjects: Barley; barley (Hordeum vulgare); Cell membranes; efflux; Elution; ion channels; membrane integrity; Plant physiology; Plant roots; Plants; Potassium; potassium transport; Salinity; salt stress; Seedlings; Sodium
• ISSN: 0028-646X; 1469-8137
• DOI: 10.1111/j.1469-8137.2009.03169.x

Stimulation of potassium (K⁺) efflux by sodium (Na⁺) has been the subject of much recent attention, and its mechanism has been attributed to the activities of specific classes of ion channels. The short-lived radiotracer ⁴²K⁺ was used to test this attribution, via unidirectional K⁺-flux analysis at the root plasma membrane of intact barley (Hordeum vulgare), in response to NaCl, KCl, NH₄Cl and mannitol, and to channel inhibitors. Unidirectional K⁺ efflux was strongly stimulated by NaCl, and K⁺ influx strongly suppressed. Both effects were ameliorated by elevated calcium (Ca²⁺). As well, K⁺ efflux was strongly stimulated by KCl, NH₄Cl and mannitol , and NaCl also stimulated ¹³NH₄⁺ efflux. The Na⁺-stimulated K⁺ efflux was insensitive to cesium (Cs⁺) and pH 4.2, weakly sensitive to the K⁺-channel blocker tetraethylammonium (TEA⁺) and quinine, and moderately sensitive to zinc (Zn²⁺) and lanthanum (La³⁺). We conclude that the stimulated efflux is: specific neither to Na⁺ as effector nor K⁺ as target; composed of fluxes from both cytosol and vacuole; mediated neither by outwardly-rectifying K⁺ channels nor nonselective cation channels; attributable, alternatively, to membrane disintegration brought about by ionic and osmotic components; of limited long-term significance, unlike the suppression of K⁺ influx by Na⁺, which is a greater threat to K⁺ homeostasis under salt stress.