K+ Transport (k+ + transport)

Distribution by Scientific Domains


Selected Abstracts


Influence of the dietary potassium content on transepithelial potassium transport in rat jejunum

JOURNAL OF ANIMAL PHYSIOLOGY AND NUTRITION, Issue 3 2000
R. Cermak
Summary In a recent study, we found that the distal rat jejunum is able to secrete K+ under in vitro conditions. The question therefore arises as to whether the small intestine might participate in K+ homeostasis. Consequently, this study examined the influence of the dietary K+ content on transepithelial K+ transport in rat jejunum. Rats were fed two diets differing in K+ content (control diet 4.0 g K+/kg, low K+ diet (LK) 0.27 g K+/kg). After a minimal feeding period of 7 days, distal jejunal sheets were mounted in Ussing chambers and unidirectional 86Rb+ fluxes (as a marker for K+ transport) were measured under short-circuit conditions. Jejunum obtained from rats fed the control diet showed a net K+ secretion of 200 nmol Rb+/h/cm2. Unidirectional Rb+ fluxes were smaller in distal jejunum from rats fed the LK diet. In these tissues, glucose-induced short-circuit current and tissue conductance were also smaller than in controls. However, net Rb+ fluxes were not significantly different in small intestine from K+ -restricted rats compared with jejunum from control animals. Based on the observation that the dietary K+ content does not affect transepithelial net K+ transport, we conclude that transcellular K+ secretion by the small intestine is not involved in K+ homeostasis. [source]


The cyclic nucleotide-gated channel, AtCNGC10, influences salt tolerance in Arabidopsis

PHYSIOLOGIA PLANTARUM, Issue 3 2008
Kun-Mei Guo
Cyclic nucleotide-gated channels (CNGCs) in the plasma membrane transport K+ and other cations; however, their roles in the response and adaptation of plants to environmental salinity are unclear. Growth, cation contents, salt tolerance and K+ fluxes were assessed in wild-type and two AtCNGC10 antisense lines (A2 and A3) of Arabidopsis thaliana (L.) Heynh. Compared with the wild-type, mature plants of both antisense lines had altered K+ and Na+ concentrations in shoots and were more sensitive to salt stress, as assessed by biomass and Chl fluorescence. The shoots of A2 and A3 plants contained higher Na+ concentrations and significantly higher Na+/K+ ratios compared with wild-type, whereas roots contained higher K+ concentrations and lower Na+/K+ ratios. Four-day-old seedlings of both antisense lines exposed to salt stress had smaller Na+/K+ ratios and longer roots than the wild-type. Under sudden salt treatment, the Na+ efflux was higher and the K+ efflux was smaller in the antisense lines, indicating that AtCNGC10 might function as a channel providing Na+ influx and K+ efflux at the root/soil interface. We conclude that the AtCNGC10 channel is involved in Na+ and K+ transport during cation uptake in roots and in long-distance transport, such as phloem loading and/or xylem retrieval. Mature A2 and A3 plants became more salt sensitive than wild-type plants because of impaired photosynthesis induced by a higher Na+ concentration in the leaves. [source]


The Na+ transporter AtHKT1;1 controls retrieval of Na+ from the xylem in Arabidopsis

PLANT CELL & ENVIRONMENT, Issue 4 2007
ROMOLA JANE DAVENPORT
ABSTRACT HKT-type transporters appear to play key roles in Na+ accumulation and salt sensitivity in plants. In Arabidopsis HKT1;1 has been proposed to influx Na+ into roots, recirculate Na+ in the phloem and control root : shoot allocation of Na+. We tested these hypotheses using 22Na+ flux measurements and ion accumulation assays in an hkt1;1 mutant and demonstrated that AtHKT1;1 contributes to the control of both root accumulation of Na+ and retrieval of Na+ from the xylem, but is not involved in root influx or recirculation in the phloem. Mathematical modelling indicated that the effects of the hkt1;1 mutation on root accumulation and xylem retrieval were independent. Although AtHKT1;1 has been implicated in regulation of K+ transport and the hkt1;1 mutant showed altered net K+ accumulation, 86Rb+ uptake was unaffected by the hkt1;1 mutation. The hkt1;1 mutation has been shown previously to rescue growth of the sos1 mutant on low K+; however, HKT1;1 knockout did not alter K+ or 86Rb+ accumulation in sos1. [source]