Effects Of ATP Sensitive potassium channel opener on the mRNA and pro- tein expressions of caspase-12 after cerebral ischemia-reperfusion in rats

Objective To investigate effects of K_ATP opener on the expressions of caspase-12 mRNA and protein, and to explore the role of endoplasmic reticulum （ER） stress pathway in the mechanism of K_ATP opener protecting against neuronal apoptosis after cerebral ischemia-reperfusion. Methods Two hundred rats were randomly divided into four groups： sham operation group, ischemia-reperfusion group, K_ATP opener group, and K_ATP blocker group. The middle cerebral artery occlusion （MCAO） model was established by intraluminal suture occlusion method; neuronal apoptosis was detected by TUNEL staining. The mRNA and protein expressions of caspase-12 were detected by semi-quantitative RT-PCR and immunohisto-chemical staining, respectively. Results In ischemia-reperfusion group, K_ATP opener group and K_ATP blocker group, the number of apoptotic cells and the mRNA and protein expressions of caspase-12 gradually increased following cerebral reperfusion, and reached the peak at 24 h. In K_ATP opener group, The number of apoptotic cells was significantly less than that in ischemia-reperfusion group and K_ATP blocker group at 12 h, 24 h, 48 h and 72 h （P 〈 0.05 or P 〈 0.01）; while the mRNA and protein levels of caspase-12 were significantly less than those in ischemia-reperfusion group and K_ATP blocker group at all times （P 〈 0.05 or P〈0.01）. There were no differences between the ischemia-reperfusion group and K_ATP blocker group at each time （P〉 0.05）. Conclusion K_ATP opener may protect neurons from apoptosis following the cerebral ischemia-reperfusion by inhibiting ER stress pathway.

Hydrogen sulfide-induced enhancement of gastric fundus smooth muscle tone is mediated by voltagedependent potassium and calcium channels in mice

AIM:To investigate the effect of hydrogen sulfide(H2S)on smooth muscle motility in the gastric fundus.METHODS:The expression of cystathionineβ-synthase(CBS)and cystathionineγ-lyase(CSE)in cultured smooth muscle cells from the gastric fundus was examined by the immunocytochemistry technique.The tension of the gastric fundus smooth muscle was recorded by an isometric force transducer under the condition of isometric contraction with each end of the smooth muscle strip tied with a silk thread.Intracellular recording was used to identify whether hydrogen sulfide affects the resting membrane potential of the gastric fundus in vitro.Cells were freshly separated from the gastric fundus of mice using a variety of enzyme digestion methods and whole-cell patch-clamp technique was used to find the effects of hydrogen sulfide on voltage-dependent potassium channel and calcium channel.Calcium imaging with fura-3AM loading was used to investigate the mechanism by which hydrogen sulfide regulates gastric fundus motility in cultured smooth muscle cells.RESULTS:We found that both CBS and CSE were expressed in the cul tured smooth muscle cel ls from the gastric fundus and that H2S increased the smooth muscle tension of the gastric fundus in mice at low concentrations.In addition,nicardipine and aminooxyacetic acid(AOAA),a CBS inhibitor,reduced the tension,whereas Nω-nitro-L-arginine methyl ester,a nonspecific nitric oxide synthase,increased the tension.The AOAA-induced relaxation was significantly recovered by H2S,and the Na HS-induced increase in tonic contraction was blocked by 5 mmol/L4-aminopyridine and 1μmol/L nicardipine.Na HS significantly depolarized the membrane potential and inhibited the voltage-dependent potassium currents.Moreover,Na HS increased L-type Ca2+currents and caused an elevation in intracellular calcium([Ca2+]i).CONCLUSION:These findings suggest that H2S may be an excitatory modulator in the gastric fundus in mice.The excitatory effect is mediated by voltagedependent potassium and L-type calcium channels.

Bisoprolol reverses down-regulation of potassium channel proteins in ventricular tissues of rabbits with heart failure

Remodeling of ion channels is an important mechanism of arrhythmia induced by heart failure （HF）. We investigated the expression of potassium channel encoding genes in the ventricles of rabbit established by volumeoverload operation followed with pressure-overload. The reversible effect of these changes with bisoprolol was also evaluated. The HF group exhibited left ventricular enlargement, systolic dysfunction, prolongation of corrected QT interval （QTc）, and increased plasma brain natriuretic peptide levels in the HF rabbits. Several potassium channel subunit encoding genes were consistently down-regulated in the HF rabbits. After bisoprolol treatment, heart function was improved significantly and QTc was shortened. Additionally, the mRNA expression of potassium channel subunit genes could be partially reversed. The down-regulated expression of potassium channel subunits Kv4.3, Kv1.4, KvLQT1, minK and Kir 2.1 may contribute to the prolongation of action potential duration in the heart of rabbits induced by volume combined with pressure overload HF. Bisoprolol could partially reverse these down-regulations and improve heart function.

Role of Voltage-gated Potassium Channels in Pathogenesis of Chronic Pulmonary Heart Disease

The influence of hypoxia on the activity of voltage-gated potassium channel in pulmonary artery smooth muscle cells （PASMCs） of rats and its roles in the pathogenesis of chronic pulmonary heart disease were investigated. Eighty male Sprague-Dawley rats were randomly allocated into control group （n=10）, acute hypoxic group （n=10）, and chronic hypoxic groups （n=60）. The chronic hypoxic groups were randomly divided into 6 subgroups （n=10 each） according to the chronic hypoxic periods. The rats in the control group were kept in room air and those in acute hypoxic group in hypoxia envi- ronmental chamber for 8 h. The rats in chronic hypoxic subgroups were kept in hypoxia environmental chamber for 8 h per day for 5, 10, 15, 20, 25, and 30 days, respectively. The mean pulmonary arterial pressure （mPAP）, right ventricular hypertrophy index （RVHI）, and the current of voltage-gated potas- sium channel （IK） in PASMCs were measured. Results showed that both acute and chronic hypoxia could decrease the IK in PASMCs of rats and the I-V relationship downward shifted to the right. And the peak Ir density at ＋60mV decreased with prolongation of hypoxia exposure. No significant difference was noted in the density oflK （at ＋60 mV） and I-V relationship between control group and chronic hy- poxic subgroup exposed to hypoxia for 5 days （P〉0.05）, but there was a significant difference between control group and chronic hypoxic subgroup exposed to hypoxia for 10 days （P〈0.05）. Significant dif- ferences were noted in the IK density （at ＋60 mV） and I-V relationships between control group and chronic hypoxic subgroups exposed to hypoxia for 20 days and 30 days （P〈0.01）. Compared with con- trol rats, the mPAP and RVHI were significantly increased after chronic exposure to hypoxia for 10 days （P〈0.05）, which were further increased with prolongation of hypoxia exposure, and there were signifi- cant differences between control group and chronic hypoxic subgroups exposed to hypoxia for 20 days and 30 days （P〈0.01）. Both the mPAP and the RVHI were negatively correlated with the density OflK （r---0.89769 and -0.94476, respectively, both P〈0.01）. It is concluded that exposure to hypoxia may cause decreased activity of voltage-gated potassium channel, leading to hypoxia pulmonary vasocon- striction （HPV）. Sustained HPV may result in chronic pulmonary hypertension, even chronic pulmonary heart disease, contributing to the pathogenesis of chronic pulmonary heart disease.

Extract from Buthus martensii Karsch is associated with potassium channels on glioma cells

Catilan extracted from Leiurus quinquestriatus is a specific ion channel blocker.It can specifically bind chloride channels of glioma cells and kill these tumor cells.The questions remain as to whether antigliomatin,the extract from scorpion venom of Buthus martensii Karsch in China,can inhibit glioma growth,and whether this inhibition is correlated with ion channels of tumor cells.The present study treated rat C6 glioma cells with 0.8,1.2,and 1.6 μg/mL antigliomatin for 20 hours.Whole-cell patch clamp technique showed that antigliomatin delayed rectifier potassium channels of C6 glioma cells.Antigliomatin inhibited tumor growth,which could potentially involve potassium channels of tumor cells.

Effects of Ginkgo biloba extracts with mirodenafil on the relaxation of corpus cavernosal smooth muscle and the potassium channel activity of corporal smooth muscle cells

In this study, we investigated the effects of a combination of Ginkgo biloba extracts （GBE） and phosphodiesterase type 5 （PDE-5） inhibitors on the muscular tone of the corpus cavernosum and potassium channel activity of corporal smooth muscle cells. Strips of corpus cavernosum from male New Zealand white rabbits were mounted in organ baths for isometric tension studies. After contraction with 1 × 10^-5 mol I^-1 norepinephrine, GBE （0.01-1 mg ml^-1） and mirodenafil （0.01-100 nmol I^-1） were added together into the organ bath. In electrophysiological studies, whole-cell currents were recorded by the conventional patch-clamp technique in cultured smooth muscle cells of the human corpus cavernosum. The corpus cavemosum was relaxed in response to GBE in a dose-dependent manner （from 0.64%±8.35% at 0.01 mg ml^-1 to 52.28%±11.42% at 1 mg ml^-1）. After pre-treatment with 0.03 mg ml^-1 of GBE, the relaxant effects of mirodenafil were increased at all concentrations, After tetraethylammonium （TEA） （1 mmol I^-1） administration, the increased effects were inhibited （P〈0.01）. Extracellular administration of GBE increased the whole-cell K^＋ outward currents in a dose-dependent fashion. The increase of the outward current was inhibited by I mmol 1-1 TEA. These results suggest that GBE could increase the relaxant potency of mirodenafil even at a minimally effective dose. The K＋ flow through potassium channels might be one of the mechanisms involved in this synergistic relaxation.

Changes of Expression of Stretch-activated Potassium Channel TREK-1 mRNA and Protein in Hypertrophic Myocardium

The expression of stretch activated potassium channel TREK-1 mRNA and protein of hypertrophic myocardium was measured. Using a model of hypertrophy induced by coarctation of abdominal aorta in male Wistar rats, the expression of TREK-1 mRNA and protein was detected by using semi quantitative RT-PCR and Western blot respectively. At 4th and 8th week after constriction of the abdominal aorta , rats developed significant left ventricular hypertrophy. As compared to sham-operated group, stretch-activated potassium channel TREK-1 mRNA was strongly expressed and protein was up regulated in operation groups （P〈0.05）. It was concluded that the expression of TREK-1 was up-regulated in hypertrophic myocardium induced by chronic pressure overload in Wistar rats.

Astrocytic Kir4.1 potassium channels as a novel therapeutic target for epilepsy and mood disorders

Astrocytic Kir4.1 channels and spatial potassium buffering：Astrocytes play a crucial role in maintaining the structural and functional integrity of the brain,which includes formation of the blood-brain barrier,maintenance of water and ion homeostasis,metabolism of neurotransmitters and secretion of various neuroactive molecules.

Adenosine triphosphate-sensitive potassium channel opener protects PC12 cells against hypoxia-induced apoptosis through PI3K/Akt and Bcl-2 signaling pathways

Although previous studies have shown the neuroprotective effects of the adenosine triphosphate （ATP）-sensitive potassium （KATP） channel opener against ischemic neuronal damage, little is known about the mechanisms involved. Phosphatidylinositol-3 kinase （PI3K）/v-akt murine thy-moma viral oncogene homolog （Akt） and Bcl-2 are thought to be important factors that mediate neuroprotection. The present study investigated the effects of KATP openers on hypoxia-induced PC12 cell apoptosis, as well as mRNA and protein expression of Akt and Bcl-2. Results demon-strated that pretreatment of PC12 cells with pinacidil, a KATP opener, resulted in decreased PC12 cell apoptosis following hypoxia, as detected by Annexin-V fluorescein isothiocyanate/ propidium iodide double staining flow cytometry. In addition, mRNA and protein expression of phosphorylated Akt （p-Akt） and Bcl-2 increased, as detected by immunofluorescence, Western blot analysis, and reverse-transcription polymerase chain reaction. The protective effect of this preconditioning was attenuated by glipizide, a selective KATP blocker. These results demonstrate for the first time that the protective mechanisms of KATP openers on PC12 cell apoptosis following hypoxia could result from activation of the PI3K/Akt signaling pathway, which further activates expression of the downstream Bcl-2 gene.

Chlorogenic acid alters the voltage-gated potassium channel currents of trigeminal ganglion neurons

Chlorogenic acid（5-caffeoylquinic acid, CGA） is a phenolic compound that is found ubiquitously in plants, fruits and vegetables and is formed via the esterification of caffeic acid and quinic acid. In addition to its notable biological functions against cardiovascular diseases, type-2 diabetes and inflammatory conditions, CGA was recently hypothesized to be an alternative for the treatment of neurological diseases such as Alzheimer＇s disease and neuropathic pain disorders. However, its mechanism of action is unclear.Voltage-gated potassium channel（Kv） is a crucial factor in the electro-physiological processes of sensory neurons. Kv has also been identified as a potential therapeutic target for inflammation and neuropathic pain disorders. In this study, we analysed the effects of CGA on the two main subtypes of Kv in trigeminal ganglion neurons, namely, the IK,Aand IK,Vchannels. Trigeminal ganglion（TRG）neurons were acutely disassociated from the rat TRG, and two different doses of CGA（0.2 and 1 mmol·L21） were applied to the cells.Whole-cell patch-clamp recordings were performed to observe alterations in the activation and inactivation properties of the IK,Aand IK,Vchannels. The results demonstrated that 0.2 mmol·L21CGA decreased the peak current density of IK,A. Both 0.2 mmol·L21and1 mmol·L21CGA also caused a significant reduction in the activation and inactivation thresholds of IK,Aand IK,V. CGA exhibited a strong effect on the activation and inactivation velocities of IK,Aand IK,V. These findings provide novel evidence explaining the biological effects of CGA, especially regarding its neurological effects.

Hypoxic pulmonary hypertension and novel ATP-sensitive potassium channel opener: the new hope on the horizon

Hypoxic pulmonary hypertension(HPH) is a syndrome characterized by the increase of pulmonary vascular tone and the structural remodeling of peripheral pulmonary arteries.The aim of specific therapies for hypoxic pulmonary hypertension is to reduce pulmonary vascular resistance,reverse pulmonary vascular remodeling,and thereby improving right ventricular function.Iptakalim,a lipophilic para-amino compound with a low molecular weight,has been demonstrated to be a new selective ATP-sensitive potassium(K ATP) channel opener via pharmacological,electrophysiological,biochemical studies,and receptor binding tests.In hypoxia-induced animal models,iptakalim decreases the elevated mean pressure in pulmonary arteries,and attenuates remodeling in the right ventricle,pulmonary arteries and airways.Furthermore,iptakalim has selective antihypertensive effects,selective vasorelaxation effects on smaller arteries,and protective effects on endothelial cells,but no effects on the central nervous,respiratory,digestive or endocrine systems at therapeutic dose.Our previous studies demonstrated that iptakalim inhibited the effects of endothelin-1,reduced the intracellular calcium concentration and inhibited the proliferation of pulmonary artery smooth muscle cells.Since iptakalim has been shown safe and effective in both experimental animal models and phase I clinical trials,it can be a potential candidate of HPH in the future.

Aberrant expression of ether à go-go potassium channel in colorectal cancer patients and cell lines

AIM: To study the expression of ether à go-go (Eag1) potassium channel in colorectal cancer and the relation- ship between their expression and clinico-pathological features. METHODS: The expression levels of Eag1 protein were determined in 76 cancer tissues with paired non- cancerous matched tissues as well as 9 colorectal adenoma tissues by immunohistochemistry. Eag1 mRNA expression was detected in 13 colorectal cancer tissues with paired non-cancerous matched tissues and 4 colorectal adenoma tissues as well as two colorectal cancer cell lines (LoVo and HT-29) by reverse transcription PCR. RESULTS: The frequency of positive expression of Eag1 protein was 76.3% (58/76) and Eag1 mRNA was 76.9% (10/13) in colorectal cancer tissue. Expression level of Eag1 protein was dependent on the tumor size, lymphatic node metastasis, other organ metastases and Dukes’ stage (P < 0.05), while not dependent on age, sex, site and degree of differentiation. Eag1 protein and mRNA were negative in normal colorectal tissue, and absolutely negative in colorectal adenomas except that one case was positively stained for Eag1 protein. CONCLUSION: Eag1 protein and mRNA are aberrantly expressed in colorectal cancer and occasionally expressed in colorectal adenoma. The high frequency of expression of Eag1 in tumors and the restriction of normal expression to the brain suggest the potential of this protein for diagnostic, prognostic and therapeutic purposes.

Migration-associated secretion of melanoma inhibitory activity at the cell rear is supported by KCa3.1 potassium channels

恶意的黑瘤，由侵略本地生长和转移的早形成描绘了，是皮癌症的最好攻击的类型。黑瘤禁止的活动(MIA ) ，由恶意的黑瘤房间藏匿了，与房间粘附受体， integrins 伪 4 尾 1 和伪 5 尾 1，便于的房间分开和转移的支持的形成交往。在现在的学习，我们证明那 MIA 分泌物被限制到移植房间的后面的目的，当在非移居的房间 MIA 在肌动朊外皮积累时。MIA 蛋白质包括上衣蛋白质建筑群拿一条常规能分泌的小径我(COPI )- 并且上衣蛋白质建筑群 II (COPII ) 依赖者蛋白质运输到房间圆周，在它的最后的版本取决于细胞内部的 Ca2+ 离子的地方。有趣地，激活 Ca2+ 的 K+ 隧道，亚科 N，成员 4 (KCa3.1 ) ，知道在移植房间的后面的结束活跃，被发现支持 MIA 分泌物。分泌物被特定的 KCa3.1 隧道禁止者 TRAM-34 并且由隧道的主导否定的异种的表示减少。在摘要，我们阐明了到房间尾部并且也的 MIA 蛋白质的联系迁居的运输揭示了 KCa3.1 钾隧道由支持房间移植的新机制。

Effect of acupuncture combined with Xijing Tongmai decoction on the sustained expression of transient outward potassium channel related protein in rats with myocardial infarction

Objective:To observe the sustained expression of transient outward potassium channel related proteins at the end of the treatment and 30 days after the end of the treatment in rats,and to explore the sustained curative effect and mechanism of acupuncture combined with Xijingtongmai decoction in rats with myocardial infarction.Methods:Twenty of 130 male SD rats were random extracted as the control group,and the rest were used to establish myocardial infarction by fed with high-fat diet and then injected with isoproterenol.According to ECG,80 rats were successfully established.Then they were randomly divided into model group,acupuncture combined with Chinese medicine group,acupuncture group and Western medicine group.The content of bFGF protein was measured by ELISA.The protein contents of Kv1.4,Kv4.2,Kv4.3 and KChIP2 were measured by Western blot.Results:At the end of treatment,compared with the model group,the protein contents of Kv1.4,Kv4.2,Kv4.3,KChIP2 and bFGF in each treatment group increased,and the increase was most significant in the acupuncture combined with Chinese medicine group(P<0.05).At the end of treatment,compared with the model group,the protein contents of Kv1.4,Kv4.2,Kv4.3,KChIP2 and bFGF in each treatment group increased,and the increase was most significant in the acupuncture combined with Chinese medicine group(P<0.05).Compared with the treatment group at the end of treatment,the expression of Kv1.4,Kv4.2,Kv4.3,KChIP2 and bFGF protein in each treatment group 30 days after the end of treatment decreased slightly(P<0.05),but still higher than that of the model group at this time(P<0.05).The combination of acupuncture and Chinese medicine group decreased the least of them(P<0.05).Conclusion:The results showed that acupuncture combined with xijingtongmai decoction had a sustained good effect.Its sustained action mechanism may be achieved by continuously increasing the protein content of Kv1.4,Kv4.2,Kv4.3,KChIP2 and bFGF through transient outward potassium channel.

Acetylcholine modulates transient outward potassium channel in acutely isolated cerebral cortical neurons of rats

BACKGROUND： The neuronal transient outward potassium channel has been shown to be highly associated with acetylcholine. However, the influence of acetylcholine on the transient outward potassium current in cerebral cortical neurons remains poorly understood. OBJECTIVE： To investigate acetylcholine modulation on transient outward potassium current in rat parietal cortical neurons using the whole-cell patch-clamp technique. DESIGN, TIME AND SETTING： A neuroelectrophysiology study was performed at the Department of Physiology, Harbin Medical University between January 2005 and January 2006. MATERIALS： Wistar rats were provided by the Animal Research Center, the Second Hospital of Harbin Medical University; PC-IIC patch-clamp amplifier and IBBClamp data collection analysis system were provided by Huazhong University for Science and Technology, Wuhan, China; PP-83 microelectrode puller was purchased from Narrishage, Japan. METHODS： The parietal somatosensory cortical neurons were acutely dissociated, and the modulation of acetylcholine （0.1, 1, 10, 100 μmol/L） on transient outward potassium channel was recorded using the whole-cell patch-clamp technique. MAIN OUTCOME MEASURES： Influence of acetylcholine on transient outward potassium current, potassium channel activation, and inactivation. RESULTS： The inhibitory effect of acetylcholine on transient outward potassium current was dose- and voltage-dependent （P 〈 0.01）. Acetylcholine was found to significantly affect the activation process of transient outward potassium current, i.e., the activation curve of transient outward potassium current was left-shifted, while the inactivation curve was shifted to hyperpolarization. Acetylcholine significantly prolonged the time constant of recovery from inactivation of transient outward potassium current （P 〈 0.01）. CONCLUSION： These results suggest that acetylcholine inhibits transient outward potassium current by regulating activation and inactivation processes of the transient outward potassium channel.

Effects of ATP-sensitive Potassium Channels on the Expression of P21, P27 and Leptin

This study investigated the effects of ATP-sensitive potassium channels on the expression of P21, P27 and leptin. The expression of receptor of ATP-sensitive potassium channels （sulphonylurea receptor, SUR） mRNA in the preadipocytes and leptin mRNA was detected by PCR after rat preadipocytes were treated with the opener （diazoxide） or inhibitor （glibenclamide） of ATP-sensitive potassium channels during the process of inducing differentiation. The expression of P21 and P27 in preadipocytes treated with diazoxide or glibenclamide was assayed by Western blot. The results showed that the expression of SUR2, not SUR1 was detected in adipose tissue, preadipocytes and adipocytes. Alter treatment of preadipocytes with diazoxide, the expression levels of P21 and P27 were obviously higher than glibenclamide-treat ed group those in control group, but the were lower than those in control expression levels of P21 and P27 in group. During the process of inducing differentiation, the expression of leptin mRNA in preadipocytes treated with diazoxide was increased greatly, but the expression of leptin mRNA in glibenclamide-treated group decreased obviously. It was concluded that ATP-sensitive potassium channels might be involved in the proliferation and differentiation of rat preadipocytes by changing the expression of P21, P27 and leptin.

Potassium channel in peripheral blood lymphocytes of turbot (Scophthalmus maximus)

In order to provide pertinent evidence of ion channel with immune response in the fish, whole cell patch-clamp technique was employed for potassium ion channel study in turbot （Scophthalmus maximus）. Lymphocytes were isolated by Percoll density gradient centrifugation from peripheral blood samples, and electrophysiological characters of the channel were analyzed. In the recorded cells, activated voltage of the channels was -42.5±3.7 mV and the average peak current was 313.12±28.2 pA. The channel was identified as voltage dependent, the current was outward and it could be inhibited by 10 mmol/dma TEA or 5 mmol/dm^3 4-AP, a specific potassium channel inhibitor, identifying the existence of potassium channel in peripheral lymphocytes of the turbot.

Characteristics of Transient Outward Potassium Channel Exposed to 3 mT Static Magnetic Field

Acutely isolated mouse hippocampal CA3 pyramidal neurons were exposed to 3 mT static magnetic field,and the characteristics of transient outward K+ channel were studied using the whole-cell patch-clamp technique.The experiment revealed that the amplitude of transient outward potassium channel current was reduced.The maximum activated current densities of control group and exposure group were 163.62±20.68 pA/pF and 98.74±16.57 pA/pF(n=12,P<0.01) respectively.The static magnetic field exposure affected the activation and inactivation process of transient outward potassium channel current.Due to the magnetic field exposure,the half-activation voltage of the activation curves changed from 5.59±1.96 mV to 27.87±7.24 mV(n=12,P<0.05) ,and the slope factor changed from 19.43±2.11 mV to 25.87±4.22 mV(n=12,P<0.05) .The half-inactivation voltage of the inactivation curves also changed from-56.09±0.89 mV to-57.16±1.10 mV(n=12,P>0.05) and the slope factor of the inactivation curves from 8.69±0.80 mV to 10.87±1.02 mV(n=12,P<0.05) .The results show that the static magnetic field can change the characteristics of transient outward K+ channel,and affect the physiological functions of neurons.

Potassium nutrition of maize:Uptake,transport,utilization,and role in stress tolerance

Potassium(K) is an essential macronutrient for plant growth and development and influences yield and quality of agricultural crops.Maize(Zea mays) is one of the most widely distributed crops worldwide.In China,although maize consumes a large amount of K fertilizer,the K uptake/utilization efficiency(KUE)of maize cultivars is relatively low.Elucidation of KUE mechanisms and development of maize cultivars with higher KUE are needed.Maize KUE is determined by K+uptake,transport,and remobilization,which depend on a variety of K+channels and transporters.We review basic information about K+channels and transporters in maize,their functions and regulation,and the roles of K+in nitrogen transport,sugar transport,and salt tolerance.We discuss challenges and prospects for maize KUE improvement.