Effects of magnetic stimulation at different frequencies on neuronal excitability and voltage-gated potassium channels / 生物医学工程学杂志

As a noninvasive neuromodulation technique, transcranial magnetic stimulation (TMS) is widely used in the clinical treatment of neurological and psychiatric diseases, but the mechanism of its action is still unclear. The purpose of this paper is to investigate the effects of different frequencies of magnetic stimulation (MS) on neuronal excitability and voltage-gated potassium channels in the

Effects of Paroxetine on a Human Ether-a-go-go-related Gene (hERG) K⁺ Channel Expressed in Xenopus Oocytes and on Cardiac Action Potential

K⁺ channels are key components of the primary and secondary basolateral Cl- pump systems, which are important for secretion from the salivary glands. Paroxetine is a selective serotonin reuptake inhibitor (SSRI) for psychiatric disorders that can induce QT prolongation, which may lead to torsades de pointes. We studied the effects of paroxetine on a human K⁺ channel, human ether-a-go-go-related gene (hERG), expressed in Xenopus oocytes and on action potential in guinea pig ventricular myocytes. The hERG encodes the pore-forming subunits of the rapidly-activating delayed rectifier K⁺ channel (I(Kr)) in the heart. Mutations in hERG reduce I(Kr) and cause type 2 long QT syndrome (LQT2), a disorder that predisposes individuals to life-threatening arrhythmias. Paroxetine induced concentration-dependent decreases in the current amplitude at the end of the voltage steps and hERG tail currents. The inhibition was concentration-dependent and time-dependent, but voltage-independent during each voltage pulse. In guinea pig ventricular myocytes held at 36℃, treatment with 0.4 µM paroxetine for 5 min decreased the action potential duration at 90% of repolarization (APD₉₀) by 4.3%. Our results suggest that paroxetine is a blocker of the hERG channels, providing a molecular mechanism for the arrhythmogenic side effects of clinical administration of paroxetine.

Effect of down-regulation of IKs repolarization-reserve on ventricular arrhythmogenesis in a guinea pig model of cardiac hypertrophy / 中南大学学报(医学版)

Objective:To observe the changes of rapidly activated delayed rectifier potassium channel (IKs) and slowly activated delayed rectifier potassium channel (IKs) in cardiac hypertrophy and to evaluate the effects of IKs and IKs blocker on the incidence ofventricular arrhythmias in guinea pigs with left ventricular hypertrophy (LVH).Methods:Guinea pigs were divided into a sham operation group and a left ventricular hypertrophy (LVH) group.LVH model was prepared.Whole cell patch-clamp technique was used to record IKr and IKs tail currents in a guinea pig model with LVH.The changes of QTc and the incidence rate of ventricular arrhythmias in LVH guinea pigs were observed by using the IKr and IKs blockers.Results:Compared with cardiac cells in the control group,the interventricular septal thickness at end systole (IVSs),left ventricular posterior wall thickness at end systole (LVPWs),QTc interval and cell capacitance in guinea pigs with LVH were significantly increased (P＜0.05);while IKs densities were significantly reduced [+60 mV:(0.36±0.03) pA/pF vs (0.58±0.05) pA/pF,P＜0.01].However,LVH exerted no significant effect on IKr densities.IKr blocker markedly prolonged the QTc interval (P＜0.01) and increased the incidence of ventricular arrhythmias in guinea pigs with LVH compared with the control guinea pigs.In contrast,IKs blocker produced modest increase in QTc interval in guinea pigs of control group with no increase in LVH animals.IKs blocker did not induce ventricular arrhythmias incidence in either control or LVH animals.Conclusion:The cardiac hypertrophy-induced arrhythmogenesis is due to the down-regulation of IKs.

Chronic Ca²⁺ influx through voltage-dependent Ca²⁺ channels enhance delayed rectifier K⁺ currents via activating Src family tyrosine kinase in rat hippocampal neurons

Excessive influx and the subsequent rapid cytosolic elevation of Ca²⁺ in neurons is the major cause to induce hyperexcitability and irreversible cell damage although it is an essential ion for cellular signalings. Therefore, most neurons exhibit several cellular mechanisms to homeostatically regulate cytosolic Ca²⁺ level in normal as well as pathological conditions. Delayed rectifier K⁺ channels (I(DR) channels) play a role to suppress membrane excitability by inducing K⁺ outflow in various conditions, indicating their potential role in preventing pathogenic conditions and cell damage under Ca²⁺-mediated excitotoxic conditions. In the present study, we electrophysiologically evaluated the response of IDR channels to hyperexcitable conditions induced by high Ca²⁺ pretreatment (3.6 mM, for 24 hours) in cultured hippocampal neurons. In results, high Ca²⁺-treatment significantly increased the amplitude of IDR without changes of gating kinetics. Nimodipine but not APV blocked Ca²⁺-induced IDR enhancement, confirming that the change of I(DR) might be targeted by Ca²⁺ influx through voltage-dependent Ca²⁺ channels (VDCCs) rather than NMDA receptors (NMDARs). The VDCC-mediated I(DR) enhancement was not affected by either Ca²⁺-induced Ca²⁺ release (CICR) or small conductance Ca²⁺-activated K⁺ channels (SK channels). Furthermore, PP2 but not H89 completely abolished I(DR) enhancement under high Ca²⁺ condition, indicating that the activation of Src family tyrosine kinases (SFKs) is required for Ca²⁺-mediated I(DR) enhancement. Thus, SFKs may be sensitive to excessive Ca²⁺ influx through VDCCs and enhance I(DR) to activate a neuroprotective mechanism against Ca²⁺-mediated hyperexcitability in neurons.

Effects of G-CSF on calcium, sodium and potassium ion channel currents of ischemic atrial myocytes in guinea pig / 中国病理生理杂志

AIM:To observe the effects of granulocyte colony-stimulating factor (G-CSF) on calcium, sodium and potassium ion channel currents of the ischemic atrial myocytes in guinea pig by whole-cell patch clamp technique.METHODS:The guinea pig atrial myocytes were obtained by enzymolysis.Under ischemia and hypoxia condition, whole-cell patch clamp was used to observe the effects of G-CSF at various concentrations on the changes of the I-V curve, activation curve and availability of L-type calcium channel current (ICa,L) and voltage-dependent sodium channel current (INa), as well as I-V curve of delayed rectifier potassium channel current (IK).RESULTS:Under ischemic condition, the I-V curves of ICa,L were changed by acute G-CSF intervention in a dose-dependent fashion.Except for G-CSF at dose of 300 μg/kg, the other concentrations of G-CSF did not change the activation curve and availability of ICa,L, indicating that the effects of G-CSF on ICa,L were in a voltage-independent fashion.The I-V curves of ICa,L under ischemic condition were gradually approaching the normal levels by the higher dose of G-CSF, while the effect of 300 μg/kg G-CSF on ICa,L was similar to 100 μg/kg G-CSF.Acute G-CSF intervention at different doses did not change I-V curve, activation curve, and availability or steady-state availability of INa.As a part of IK, the rapid activating component (IKr) was improved by 100 μg/kg and 300 μg/kg G-CSF intervention with the similar effects, while the slowly activating component (IKs) was not changed by G-CSF.CONCLUSION:G-CSF affects ion channel electrophysiological properties of ischemic atrial myocytes in a voltage-independent but concentration-dependent manner, thus reducing the incidence of atrial arrhythmia.

Effects of retinal ganglion cell apoptosis on delayed rectifier K+currents / 中国病理生理杂志

AIM: To investigate the effects of rat retinal ganglion cell (RGC) apoptosis on delayed rectifier K+currents (IK).METHODS:The retinas of 2~3 d newborn Sprague-Dawley rats were dissociated into cell suspension by trypsin digestion .The RGCs were cultured and divided into control group , pressure 0.5 h group, pressure 1 h group, pressure 1.5 h group and pressure 2 h group.The cells were cultured regularly for 6 d in control group , and the cells in other groups were cultured regularly for 6 d and gave pressure of 80 mmHg for 0.5 h, 1 h, 1.5 h and 2 h, respectively. The rhodamine 123 fluorescence from labeled RGC mitochondrion was detected by continuous wavelength multifunctional microplate detection instrument.The membrane capacitance (Cm) in different groups and IK in the pressure 1 h group were recorded from the RGCs by whole-cell patch-clamp technique .RESULTS:No difference of rhodamine 123 fluorescence in the RGC mitochondria between control group and pressure 0.5 h group was observed .Rhodamine 123 fluorescence in the other 3 groups was significantly lower than that in control group (P<0.05).No difference of the Cm between control group and pressure 0.5 h group was found, and the Cm in the other 3 groups was significantly lower than that in control group (P<0.05).The amplitudes of IK were higher than that in control group .At the test potential from -10 mV to 60 mV, the current density in pressure 1 h group was significantly higher than that in control group (P<0.05).The maximal conduc-tion ( Gmax ) in pressure 1 h group was significantly higher than that in control group .The voltage for IK channel half-activa-tion ( V1/2 ) in pressure 1 h group declined comparison with control group ( P<0.01 ) , and the k value had no significant difference between the 2 groups.CONCLUSION:Retinal ganglion cell apoptosis accompanies with delayed rectifier K +current enhancement .

Voltage-gated potassium channels in cognitive dysfunction / 医学研究生学报

The growing number of cognitive dysfunction patients is bringing heavy mental and financial burdens to the society and families.Voltage-gated potassium channels (Kv), which consist of delayed rectifier potassium channels and transient outward po -tassium channels , are involved in the incidence of cognitive dysfunction .This review summarized the role of Kv channels in cognitive dysfunction and their relationship with N-methyl-D-aspartic acid receptors ( NMDARs) that play an important role in the process of learning and memory .

Response of I(Kr) and hERG Currents to the Antipsychotics Tiapride and Sulpiride

The human ether-a-go-go-related gene (hERG) channel is important for repolarization in human myocardium and is a common target for drugs that prolong the QT interval. We studied the effects of two antipsychotics, tiapride and sulpiride, on hERG channels expressed in Xenopus oocytes and also on delayed rectifier K+ currents in guinea pig cardiomyocytes. Neither the amplitude of the hERG outward currents measured at the end of the voltage pulse, nor the amplitude of hERG tail currents, showed any concentration-dependent changes with either tiapride or sulpiride (3~300 micrometer). However, our findings did show that tiapride increased the potential for half-maximal activation (V(1/2)) of HERG at 10~300 micrometer, whereas sulpiride increased the maximum conductance (G(max)) at 3, 10 and 100 micrometer. In guinea pig ventricular myocytes, bath applications of 100 and 500 micrometer tiapride at 36degrees C blocked rapidly activating delayed rectifier K+ current (I(Kr)) by 40.3% and 70.0%, respectively. Also, sulpiride at 100 and 500 micrometer blocked I(Kr) by 38.9% and 76.5%, respectively. However, neither tiapride nor sulpiride significantly affected the slowly activating delayed rectifier K+ current (I(Ks)) at the same concentrations. Our findings suggest that the concentrations of the antipsychotics required to evoke a 50% inhibition of IKr are well above the reported therapeutic plasma concentrations of free and total compound.

Effect of methylamphetamine on action potential and delayed rectifier potassium current in guinea-pig ventricular myocytes / 中国药理学与毒理学杂志

OBJECTIVE To explore the mechanism of methylamphetamine (MA) on heart toxicity. METHODS The effects of MA on delayed rectifier potassium current (IK) and action potential (AP) were analyzed in isolated decreased AP from 121.6 to 106.0 mV and delayed the action potential duration (APD), but had no effect on the resting potential. The 10%, 25%, 50%, 75% and 90% of APD (APD10, APD25, APD50, APD75 and APD90)inhibited the membrane potential of rapidly activating delayed rectifier potassium current (IKr) and slowly activating delayed rectifier potassium current (IKs), downward shifted the Ⅰ -Ⅴ curve, but had no effect on the curve shape and could be partly recovered after flushing. The tail current IKr was blocked concentration-dependently after simiarly inhibited by MA. CONCLUSION MA has inhibitory effects on Ik and AP in ventricular myocytes,which may be one of the possible electrophysiological mechanisms of the cardiac damage caused by MA.

A Carbohydrate Fraction, AIP1, from Artemisia Iwayomogi Reduces the Action Potential Duration by Activation of Rapidly Activating Delayed Rectifier K+ Channels in Rabbit Ventricular Myocytes

We investigated the effects of a hot-water extract of Artemisia iwayomogi, a plant belonging to family Compositae, on cardiac ventricular delayed rectifier K+ current (I(K)) using the patch clamp technique. The carbohydrate fraction AIP1 dose-dependently increased the heart rate with an apparent EC(50) value of 56.1+/-5.5 microgram/ml. Application of AIP1 reduced the action potential duration (APD) in concentration-dependent fashion by activating I(K) without significantly altering the resting membrane potential (IC(50) value of APD(50): 54.80+/-2.24, IC(50) value of APD(90): 57.45+/-3.47 microgram/ml). Based on the results, all experiments were performed with 50 microgram/ml of AIP1. Pre-treatment with the rapidly activating delayed rectifier K+ current (I(Kr)) inhibitor, E-4031 prolonged APD. However, additional application of AIP1 did not reduce APD. The inhibition of slowly activating delayed rectifier K+ current (I(Ks)) by chromanol 293B did not change the effect of AIP1. AIP1 did not significantly affect coronary arterial tone or ion channels, even at the highest concentration of AIP1. In summary, AIP1 reduces APD by activating I(Kr) but not I(Ks). These results suggest that the natural product AIP1 may provide an adjunctive therapy of long QT syndrome.

Block of hERG K+ Channel by Classic Histamine H1 Receptor Antagonist Chlorpheniramine

Chlorpheniramine is a potent first-generation histamine H1 receptor antagonist that can increase action potential duration and induce QT prolongation in several animal models. Since block of cardiac human ether-a-go-go-related gene (hERG) channels is one of leading causes of acquired long QT syndrome, we investigated the acute effects of chlorpheniramine on hERG channels to determine the electrophysiological basis for its proarrhythmic potential. We examined the effects of chlorpheniramine on the hERG channels expressed in Xenopus oocytes using two-microelectrode voltage-clamp techniques. Chlorpheniramine induced a concentration-dependent decrease of the current amplitude at the end of the voltage steps and hERG tail currents. The IC50 of chlorpheniramine-dependent hERG block in Xenopus oocytes decreased progressively relative to the degree of depolarization. Chlorpheniramine affected the channels in the activated and inactivated states but not in the closed states. The S6 domain mutations Y652A and F656A partially attenuated (Y652A) or abolished (F656A) the hERG current block. These results suggest that the H1 antihistamine, chlorpheniramine is a blocker of the hERG channels, providing a molecular mechanism for the drug-induced arrhythmogenic side effects.

The Study of K Channels in Smooth Muscle Cells of Rabbit Seminal Vesicle / 대한남성과학회지

PURPOSE: Ionic currents in smooth muscle have fundamental roles in initiation and maintenance of excitability and contractile status. So we studied and characterized potassium ion channels in smooth muscle cells of rabbit seminal vesicle. MATERIALS AND METHODS: Single smooth muscle cells of New Zealand White rabbit seminal vesicle were obtained using proteolytic enzymes (collagenase and papain). Using single cell and channel recording methods of patch clamp, potassium channels in smooth muscle of seminal vesicle were recorded. RESULTS: Potassium currents recorded whole-cell patch clamp method were divided into maxi-K channel dominant cells (n=11) and the cells with mixture of maxi-K and delayed rectifier K channels (n=7). Inside-out mode of patch clamp technique was used to characterize the maxi-K channel. The channel showed outward rectification and Ca-dependency. The single channel conductance of this channel estimated from slope conductance was 188 pS in physiological condition. These characters were typical properties of maxi-K channel. CONCLUSIONS: From these results it is suggested that maxi-K channel was predominantly distributed in rabbit seminal vesicle cell. The physiological roles of this channel in modulating seminal vesicle smooth muscle tone need further studies.

Characterization of Ionic Currents in Human Neural Stem Cells

The profile of membrane currents was investigated in differentiated neuronal cells derived from human neural stem cells (hNSCs) that were obtained from aborted fetal cortex. Whole-cell voltage clamp recording revealed at least 4 different currents: a tetrodotoxin (TTX)-sensitive Na+ current, a hyperpolarization-activated inward current, and A-type and delayed rectifier-type K+ outward currents. Both types of K+ outward currents were blocked by either 5 mM tetraethylammonium (TEA) or 5 mM 4-aminopyridine (4-AP). The hyperpolarization-activated current resembled the classical K+ inward current in that it exhibited a voltage-dependent block in the presence of external Ba2+ (30micrometer) or Cs+ (3micrometer). However, the reversal potentials did not match well with the predicted K+ equilibrium potentials, suggesting that it was not a classical K+ inward rectifier current. The other Na+ inward current resembled the classical Na+ current observed in pharmacological studies. The expression of these channels may contribute to generation and repolarization of action potential and might be regarded as functional markers for hNSCs-derived neurons.

Lithium Carbonate Modulation of Delayed Rectifier Potassium Channel Involves Protein Kinase C/Mitogen-activated Protein Kinase Signaling in Hippocampus of Rats / 生物化学与生物物理进展

Lithium carbonate could be used to treat or prevent brain damage following traumatic injury and neurodegenerative diseases.It has been shown that its protective effect is related to protein kinase C (PKC) and extracellular signal-related kinase (ERK).It was demonstrated that PDBu,a PKC activator,inhibited amplitudes of delayed rectifier potassium current (It,) and produced a hyperpolarizing shift in the activation-voltage curve.The responses to PDBu were inhibited by lithium carbonate (50μmol/L).Further studies showed that when pretreated with MEK/ERK inhibitor U0126 (20 μmol/L),although PDBu significantly reduced IK,lithium did not reverse the effect of PDBu.Thus,the results suggested that PKC signaling cascades,along with MAPK (mitogen-activated protein kinase) pathway,were required in the phosphorylation of potassium channel,which was presented by regulation of potassium channel characteristic.AC-cAMP and their eross-talk with GC-cGMP pathway could also modulate the effect of lithium on PKC activation,which could be one of underlying mechanisms likely related to neuroprotective effect of lithium.

Effect of Interleukin-1βon IA and IK Currents in Cultured Murine Trigeminal Ganglion Neurons / 华中科技大学学报（医学）（英德文版）

To investigate the effect of interleukin-1β (IL-1β) on IA and IK currents in cultured murine trigeminal ganglion (TG) neurons, whole-cell patch clamp technique was used to record the IA and IKcurrents before and after 20 ng/mL IL-1β perfusion. Our results showed that 20 ng/mL IL-1β inhibited IA currents (18.3±10.7)% (n=6, P＜0.05). IL-1β at 20 ng/mL had no effect on G-V curve of IA but moved the H-infinity curve V0.5 from -36.6 ± 6.1 mV to-42.4 ±5.2 m V (n=5, P＜0.01). However, 20 ng/mL IL-1β had effect on neither the amplitude nor the G-V curve of IK. IL-1β was found to selectively inhibit IA current in TG neurons and the effect may contribute to hyperalgesia under various inflammatory conditions.

The Effects of Protein Kinase C (PKC) on the Tension of Normal and Passively Sensitized Human Airway Smooth Muscle and the Activity of Voltage-dependent Delayed Rectifier Potassium Channel (Kv) / 华中科技大学学报（医学）（英德文版）

The effects of protein kinase C (PKC) on the tension and the activity of voltage-dependent delayed rectifier potassium channel (Kv) were examined in normal and passively sensitized human airway smooth muscle (HASM), by measuring tones and whole-cell patch clamp techniques, and the Kv activities and membrane potential (Em) were also detected. The results showed that phorbol 12-myristate 13-acetate (PMA), a PKC activator, caused a concentration-dependent constriction in normal HASM rings. The constriction of the passively sensitized muscle in asthma serum group was significantly higher than that of the normal group (P＜0.05), and the constrictions of both groups were completely abolished by PKC inhibitor Ro31-8220 and calcium channel inhibitor nifedipine. Kv activities of HASM cells were significantly inhibited by PMA, and the Em became more positive, as compared with the DMSO (a PMA menstruum)-treated group (P＜0.01). This effect could be blocked by Ro31-8220 (P＜0.01). It was concluded that activation of PKC could increase the tones of HASM, which might be related to the reduced Kv activity. In passively sensitized HASM rings, this effect was more notable.

The Effects of Botulinum Toxin-A on Calcium Channel and KDR Channel of the Detrusor Muscle in Rat Bladder Body / 대한비뇨기과학회지

PURPOSE: Botulium toxin-A (BoTx A) is useful in treating detrusor-sphincter dyssynergia, detrusor hyperreflexia, and refractory overactive bladder. Only the blocking action of acetycholine (ACh) release from nerve endings is the well known aspect of the action mechanism. The aim of this study is to investigate the effects of BoTx A on the detrusor muscle itself. MATERIALS AND METHODS: Sprague-Dawley rats were divided into 3 groups: the control group, the low dose injection group (1unit/ml of BoTx A, 0.5cc), and the high dose injection group (5units/ml of BoTx A, 0.5cc). All rats were either injected with normal saline (control group) or BoTx A (injection groups). Ten days after injection, a strip of the detrusor muscle was harvested. Contraction and relaxation responses of the strips were measured by an isometric force transducer. Contractions were induced by various concentrations of ACh, bethanechol, phenylephrine (PE), high concentrations of potassium (35, 70, 105, 140mM), tetraethylammonium (TEA, 0.1, 1, 10mM), 4-aminopyridine (4-AP, a delayed rectifier K+ antagonist, 0.1, 1, 10mM), and Bay K8644 (a L-type voltage dependent calcium channel opener, 0.1, 1, 10mM). The results were analyzed by ANOVA and the Student's t test. RESULTS: Contractions of the strips were noted when concentrations were above 1mM for TEA and above 0.1mM for 4-AP. A high dose injection as well as a low dose injection of BoTx A had no significant effects on the Ach or bethanechol-induced contractions of the strips compared to the control group. Denervation supersensitivity was not found in the injection groups after the Ach and bethanechol treatments, but the contractility was decreased in high concentrations of potassium (70, 105, 100mM), TEA (10mM), 4-AP (10mM), and Bay K8644 in both the high and low dose injection groups. There was no significant difference in the decrease of contractility between the high and low dose groups with the exception of the Bay K8644 1M treatment. CONCLUSIONS: BoTx seems to have some direct effects on decreasing the contractility of the detrusor muscle by increasing the delayed rectifier K+ channel activity and decreasing the L-type voltage dependent calcium channel activity.

The Effect of Propofol on Outward K+ Currents in Canine Colonic Myocytes / 대한마취과학회지

BACKGROUND: Propofol (2,6-diisopropylphenol) is a widely used intravenous anesthetic, and the effects of propofol on several ion channels have been studied at the whole cell and single-channel levels. However, in general there is no report on the effect of propofol on outward K+ currents in canine colonic myocytes, in which there are two types of outward K+ currents, a large-conductance Ca2+-activated K+ current and a classical delayed rectifier K+ current. We examined the effects of propofol on the two types of outward K+ currents the kinetics involved. METHODS: Experiments were performed on freshly dispersed smooth muscle cells from the circular muscle layer of the proximal canine colon. Outward currents were recorded using the patch clamp technique in the whole cell configuration. RESULTS: The application of propofol (600 nM-600microM) decreased net outward current in a dose-dependent manner. Propofol (6-60microM) also decreased peak delayed rectifier K+ currents. Pretreatment with TEA abolished propofol effects on delayed rectifier K+ currents. However, propofol still decreased delayed rectifier K+ currents in the presence of 4-AP. CONCLUSIONS: These data suggest that propofol decrease net outward K+ currents primarily by inhibiting large-conductance Ca2+-activated K+ currents and 4-AP resistant delayed rectifier K+ currents. These results suggest that propofol action on outward currents may depend on the different blocking mechanisms of the different types of K+ channels. If propofol cannot induce contraction, Ca2+ currents in colonic myocytes warrant further study.

Expression of delayed rectifier potassium channels in AGS cells and the effects of down-regulation of Kv1.5 on AGS cell proliferation / 解放军医学杂志

Objective To study the expression of 9 delayed rectifier potassium channel subunits in human gastric cancer cell line AGS, as well as the effect of down-regulation of the expression of Kv1.5 on AGS cells proliferation. Methods RT-PCR technique was employed to detect the mRNA expression of Kv1.1, Kv1.2, Kv1.3, Kv1.5, Kv1.6, Kv2.1, Kv2.2, Kv3.1 and Kv3.2 in AGS cells. Once the expression of Kv1.5 protein was confirmed by immunofluorescence, small interference RNA (siRNA) was applied to down-regulate the Kv1.5 protein expression, then MTT assay and flow cytometry were used to observe the cell proliferation and the cell cycle distribution. Results Totally 7 delayed rectifier potassium channel subunits were detected in AGS cells, among them the mRNA levels of Kv1.3, Kv1.5 and Kv2.1 were much higher than that of the others. It was confirmed by immunofluorescence that the Kv1.5 protein was expressed mainly in AGS cytomembrane. After the endogenous Kv1.5 expression in AGS cells was down regulated by siRNA, the cell proliferation obviously slowed down and the cell growth stopped in G1 period. Conclusion Multiform expression of delayed rectifier potassium channel subunits existed in AGS cells, and Kv1.5 may be involved in the regulation of gastric carcinoma cell proliferation by modulating the cell cycle.

Role of three kinds of potassium channel in airway hyperresponsiveness of asthmatic guinea pigs / 中国病理生理杂志

AIM: To investigate the role of Ca2+ - activated, delayed - rectifier and ATP sensitive K+ channel (KCa, Kdr, KATP) in airway hyperresponsiveness of asthmatic guinea pigs. METHODS: The method of recording the tone of isolated trachea rings was performed, and the changes of dose-response curves of trachea rings to histamine caused by different K+ channel blockade were investigated. RESULTS: (1) After inhibition of KCa, by tetraethylammonium (TEA) , the dose - response curve of trachea rings to histamine did not change in control group, while the maximal contraction of trachea rings to 10-4 mol/L and 10-3 mol/L histamine decreased significantly ( P