Effects of allitridum on rapidly delayed rectifier potassium current in HEK293 cell line / 南方医科大学学报

<p><b>OBJECTIVE</b>To study the effect of allitridum on rapidly delayed rectifier potassium current (IKr) in HEK293 cell line.</p><p><b>METHODS</b>HEK293 cells were transiently transfected with HERG channel cDNA plasmid pcDNA3.1 via Lipofectamine. Allitridum was added to the extracellular solution by partial perfusion after giga seal at the final concentration of 30 µmol/L. Whole-cell patch clamp technique was used to record the HERG currents and gating kinetics before and after allitridum exposure at room temperature.</p><p><b>RESULTS</b>The amplitude and density of IHERG were both suppressed by allitridum in a voltage-dependent manner. In the presence of allitridum, the peak current of IHERG was reduced from 73.5∓4.3 pA/pF to 42.1∓3.6 pA/pF at the test potential of +50 mV (P<0.01). Allitridum also concentration-dependently decreased the density of the IHERG. The IC50 of allitridum was 34.74 µmol/L with a Hill coefficient of 1.01. Allitridum at 30 µmol/L caused a significant positive shift of the steady-state activation curve of IHERG and a markedly negative shift of the steady-state inactivation of IHERG, and significantly shortened the slow time constants of IHERG deactivation.</p><p><b>CONCLUSION</b>Allitridum can potently block IHERG in HEK293 cells, which might be the electrophysiological basis for its anti-arrhythmic action.</p>

Electrophysiology mechanisms of 4-butyl-alpha-agarofuran: a new anxiolytic and antidepressant drug / 药学学报

To investigate the electrophysiology mechanisms of new anxiolytic and antidepressant drug: 4-butyl-alpha-agarofuran (AF-5), patch clamp-recording was used to test the effects of AF-5 on voltage-dependent sodium currents, voltage-dependent potassium currents, L-type voltage-dependent calcium currents and GABA dependent Cl(-) currents in primary cultured rat cortical neurons. Effects of AF-5 on Kv2.1 currents, expressed stably in HEK293 cells, were also tested. Our results showed that, delayed rectifier potassium currents (I(K(DR, L-type voltage-dependent calcium currents (I(LC-ca)) in primary cultured rat cortical neurons and Kv2.1 currents in HEK293 cells were significantly inhibited by AF-5, with IC50 as 6.17, 4.4 and 5.29 micromol x L(-1) respectively. However, voltage-dependent sodium currents (I(Na)), GABA dependent Cl(-) currents and transient outward potassium currents (I(K(A)) in primary cultured rat cortical neurons were not significantly blocked by AF-5. Our results concluded that, blocked I(K(DR)) and I(L-Ca) currents may be one of the mechanisms of anxiolytic and antidepression actions of AF-5.

Effect of GBE50 on delayed rectifier potassium current of ventricular myocytes in ischemic guinea pig / 中国应用生理学杂志

<p><b>OBJECTIVE</b>Ginkgo biloba extract 50 (GBE50) is a new multicomponent drug with a polyvalent action extracted from the leave of Ginkgo biloba. The aim of this experiment was to study the effects of GBE50 on delayed rectifier potassium current (I(K)) in ventricular myocytes under normal and simulated ischemia conditions in guinea pigs.</p><p><b>METHODS</b>Single ventricular myocytes were isolated by an enzymatic dissociation method. I(K) were recorded by whole-cell patch clamp technique in voltage clamp mode. GBE50 was added to the perfusion chamber from low to high concentrations (25, 50,100 mg/L) in normal condition. Different concentrations of GBE50 (25, 50, 100 mg/L) were prepared with simulated ischemic fluid.</p><p><b>RESULTS</b>(1) Under normal condition, 100 mg/L GBE50 decreased I(K) (n = 7, P < 0.05). (2) Under ischemia condition, it was observed that I(K) was inhibited (n = 8, P < 0.05). (3) Perfusion with ischemia solution containing 50 mg/L (n = 8, P > 0.05) and 100 mg/L GBE50 (n = 6, P > 0.05) could reverse the decrease of I(K).</p><p><b>CONCLUSION</b>GBE50 significantly decreased I(K) in a concentration-dependent manner. GBE50 could alleviate the electrophysiological heterogeneity of myocardium to prevent ischemic myocardium from arrhythmia.</p>

Effect of etomidate on voltage-dependent potassium currents in rat isolated hippocampal pyramidal neurons / 中华医学杂志(英文版)

<p><b>BACKGROUND</b>Previous studies demonstrated general anesthetics affect potassium ion channels, which may be one of the mechanisms of general anesthesia. Because the effect of etomidate on potassium channels in rat hippocampus which is involved in memory function has not been studied, we investigated the effects of etomidate on both delayed rectifier potassium current (I(K(DR))) and transient outward potassium current (I(K(A))) in acutely dissociated rat hippocampal pyramidal neurons.</p><p><b>METHODS</b>Single rat hippocampal pyramidal neurons from male Wistar rats of - 10 days were acutely dissociated by enzymatic digestion and mechanical dispersion according to the methods of Kay and Wong with slight modification. Voltage-clamp recordings were performed in the whole-cell patch clamp configuration. Currents were recorded with a List EPC-10 amplifier and data were stored in a computer using Pulse 8.5. Student's paired two-tail t test was used for data analysis.</p><p><b>RESULTS</b>At the concentration of 100 micromol/L, etomidate significantly inhibited I(K(DR)) by 49.2% at +40 mV when depolarized from -110 mV (P < 0.01, n = 8), while did not affect I(K(A)) (n = 8, P > 0.05). The IC(50) value of etomidate for blocking I(K(DR)) was calculated as 5.4 micromol/L, with a Hill slope of 2.45. At the presence of 10 micromol/L etomidate, the V1/2 of activation curve was shifted from (17.3 +/- 1.5) mV to (10.7 +/- 2.9) mV (n = 8, P < 0.05), the V1/2 of inactivation curve was shifted from (-18.3 +/- 2.2) mV to (-45.3 +/- 9.4) mV (n = 8, P < 0.05). Etomidate 10 micromol/L shifted both the activation curve and inactivation curve of I(K(DR)) to negative potential, but mainly affected the inactivation kinetics.</p><p><b>CONCLUSIONS</b>Etomidate potently inhibited I(K(DR)) but not I(K(A)) in rat hippocampal pyramidal neurons. I(K(DR)) was inhibited by etomidate in a concentration-dependent manner, while I(K(A)) remained unaffected.</p>

Dynamic changes of electrical remodeling in midmyocardium of rabbit left ventricle during the early stage of chronic pressure-overload / 生理学报

In the previous study, we had found that the action potential duration (APD) of midmyocardial (M) cells was gradually prolonged and M cells were easier to produce early after-depolarization (EAD) in the rabbit left ventricle during the early stage of chronic pressure-overload. The present study was performed to investigate the dynamic changes and significance of ionic current remodeling in M cells of rabbit left ventricle during the early stage of chronic pressure-overload. Sixty-four New Zealand rabbits were randomly divided into constriction groups and sham groups. The rabbit models with chronic pressure-overload were prepared by partial constriction of suprarenal abdominal aorta at the site proximal 5-10 mm away from the left renal artery. At 2 and 8 weeks after operation, the single cardiomyocytes were isolated by enzymatic digestion method. The midmyocardium from the anterolateral free wall of left ventricle was obtained by removing the epicardial and endocardial surfaces. Whole-cell patch-clamp technique was used to record the slowly activating delayed rectifier potassium current (I(Ks)), transient outward potassium current (I(to)), L-type calcium current (I(Ca-L)) of M cells. At 2 weeks after the constriction operation, compared with the sham group, I(Ks) tail current (I(Ks,tail)) and I(to) densities of M cells from constriction group significantly decreased by 33.3% and 51.5%, respectively. There was no significant difference in I(Ca-L) density between the two groups. At 8 weeks after operation, compared with the sham group, I(Ks,tail) and I(to) densities of M cells from constriction group significantly decreased by 37.0% and 49.2%, respectively. There was still no significant difference in I(Ca-L) density between the two groups. These results suggest that during the early phase of chronic pressure-overload, the electrical remodeling of M cells in rabbit left ventricle has developed, representing as the down regulations of I(Ks) and I(to) that can lead to the prolongation of APD, which might be a risk factor for the occurrence of malignant arrhythmia.

The effects of Sphing-1-phosphate(S1P) on the potassium channel of the ventricular myocytes / 中国应用生理学杂志

<p><b>AIM</b>To study the effect of Sphingosine-1-phosphate on the delayed rectifier potassium current (IK) and the inward rectifier potassium current (IK1) of guinea pig isolated ventricular myocytes.</p><p><b>METHODS</b>Whole cell patch clamp technique was applied to record the delayed rectifier potassium current and the delayed rectifier potassium current of guinea pig isolated ventricular myocytes.</p><p><b>RESULTS</b>(1) IK of S1P (1.1 micromol/L) decreased from (1.2 +/- 0.26)nA to (0.95 +/- 0.23)nA. While IK of S1P (2.2 micromol/L) decreased from (1.43 +/- 0.31)nA to (1.02 +/- 0.28)nA. There was significant difference compared to control group (P < 0.01, n = 6). The IK peak value was decreased from (1.29 +/- 0.26) nA to (1.26 +/- 0.37)nA at the group of S1P (1.1 micromol/L) plus suramin (200 micromol/L) and showed no significant difference compared to control group (P > 0.05, n = 6). (2) IK1 of S1P (1.1 micromol/L) decreased from (-8.94 +/- 2.01)nA to (-8.81 = 1.55)nA. While IK of S1P (2.2 micromol/L) decreased from (-8.86 +/- 1.59)nA to (-8.55 +/- 1.39)nA. There was no significant difference compared to control group (P > 0.05, n = 6).</p><p><b>CONCLUSION</b>S1P inhibits delayed rectifier potassium current of ventricular myocyte in guinea pig remarkably, S1P shows no effects on delayed rectifier potassium current of ventricular myocyte in guinea pig.</p>

Two-way concentration-dependent effect of H2O2 on I(Kur) and I(Ca,L) in human atrial myocytes / 生理学报

It has been shown that oxidative stress correlates with atrial fibrillation (AF). The purpose of the present study was to investigate the effects of reactive oxygen species (ROS) on the electrophysiological activity of human atrial myocytes. Right atrial appendages were obtained from patients with AF (AF group, n=12) and without AF (non-AF group, n=12). Single human atrial myocytes were isolated through enzymatic dissociation with type XXIV protease and type V collagenase, then divided into three subgroups: control group (n=12), H2O2 group (0.1, 0.2, 0.5, 0.75, 1, 2, 5, 10 mumol/L, n=7 at each concentration) and vitamin C (antioxidant) group (1 mumol/L, n=7). Ultrarapid delayed rectifier K(+) current (I(Kur)), L-type calcium current (I(Ca,L)) and action potential duration (APD) were recorded by whole-cell patch clamp. In AF control group, the maximum current densities of I(Kur) and I(Ca,L) were significantly lower than that in non-AF control group (both P<0.05) and APD(90) was significantly shorter as well (P<0.05). In both non-AF and AF groups, H2O2 showed two-way concentration-dependent effect on I(Kur) and I(Ca,L). The maximum current densities of I(Kur) and I(Ca,L) was significantly increased at lower H2O2 concentration, but was decreased at higher H2O2 concentration. In non-AF group, 0.2 mumol/L H2O2 caused a peak increase in the maximum current identities of I(Kur) [(8.92+/-0.51) pA/pF, P<0.05] and I(Ca,L) [(9.32+/-0.67) pA/pF, P<0.05]. H2O2 at a concentration higher than 0.75 mumol/L decreased I(Kur) and I(Ca,L). When the H2O2 concentrations were 0.2, 1, 2, 5 and 10 mumol/L, APD(90) was significantly shorter compared with that in non-AF control group (P<0.05), meanwhile it had no significant difference from that in AF control group. In AF group, the peak effective concentration of H2O2 was 0.5 mumol/L, and the turning concentration was 1 mumol/L. The H2O2 concentration-current density curve in AF group was similar to that in non-AF group, but the turning point shifted to the right, indicating that the way that H2O2 acted on ion channels in AF was the same as that in non-AF, however, the sensitivity of ion channels to H2O2 was decreased in AF. Vitamin C reversed these changes induced by H2O2, and did not affect the characteristics of ion channels. H2O2-induced electrophysiological changes in human atrial myocytes were similar to atrial electrical remodeling (AER) in AF, suggesting that ROS might induce AF. Meanwhile, H2O2 also could aggravate AER in AF, contributing to the maintenance of AF. The results suggest that antioxidants might play a significant role in the prevention and treatment of AF.

The change of potassium current of neural stem cells cultured in vitro from newborn rat hippocampus / 中国应用生理学杂志

<p><b>AIM</b>To observe the change of potassium current on cultured neurons differentiated from hippocampus neural stem cells of the newborn rat.</p><p><b>METHODS</b>Neural stem cells from newborn rat hippocampus were cultured in vitro and passaged continuously. Differentiation of the cell was induced by serum and removing mitogens. After differentiation cells were plated on plastic dishes and cultured for 1 d, 7 d, 14 d and 21 d. Whole-cell voltage patch clamp recording was used respectively to detect voltage-dependent K+ current.</p><p><b>RESULTS</b>After 1 d culture, no current was detected, and on the 7th d, 14th d, 21st d after differentiation, the amplitude of K+ currents was (18.077 +/- 2.789)pA/pF, (13.099 +/- 2.742)pA/pF, (34.045 +/- 8.067)pA/pF at +50 mV. The recorded K+ current included two components that could be blocked by TEA and 4-AP separately, assumed the slowly inactivating delayed rectifier K+ current (IK) and the fast inactivating transient outward K+ current (IA).</p><p><b>CONCLUSION</b>The function of potassium channels on the hippocampus neural stem cells of the newborn rat approaches mature gradually when the time of differentiation becomes longer in vitro.</p>

Inhibition of ACh on the delayed rectifier-like potassium current in acutely isolated cerebral cortical neurons of rats / 生理学报

The modulation of ACh on delayed rectifier-like potassium currents (I(K)) was studied in freshly dissociated cerebral cortical neurons using the whole-cell patch-clamp technique. Wistar rats between 10- and 14-day old of both sexes were used. After rats were decapitated, their brains were quickly removed, iced, and then manually cut into 400 mum slices. Slices were then incubated for 0.5 h at 32 degrees C in a buffered artificial cerebrospinal fluid (ACSF) bubbled with 95% O2, 5% CO2. Slices were then removed into buffered ACSF containing protease (0.5 mg/ml) at 32 degrees C. After 30 min of enzyme digestion, tissue was rinsed three times in the buffered saline. Then the enzyme-treated slices were mechanically dissociated with a graded series of fire-polished Pasteur pipettes. The cell suspension was then plated into a 35 mm dish and placed on the stage of a Olympus inverted microscope. For whole-cell recordings of currents, standard voltage-clamp techniques were used. Neurons were held at -80 mV, and the I(K) was evoked by 2 000 ms depolarizing voltage commands to potential between -40 mV and +60 mV in 10 mV steps applied at a frequency of 0.5 Hz. It was found that the inhibitory effect of ACh (0.1, 1, 10, 100 mumol/L) on I(K) was dose-dependent. It was also found that ACh affected the activation process of I(K) significantly, i.e., the activation curve of I(K) was characterized by half-activation potential of (-41.8+/-9.7) mV and a slope factor of (30.7+/-7.2) mV in the cortical neurons and they were changed to (-122.4+/-38.6) mV and (42.4+/-7.0) mV, respectively, after giving ACh (10 mumol/L). Tubocurarine (100 mumol/L) antagonized the inhibitory effect of ACh on I(K), and the drop of currents varied from the control value of (36.5+/-7..8)% to (16.9+/-13.8)% (n=8, P<0.01). 4-DAMP (10 mumol/L) blocked the inhibitory effect of ACh on I(K), and the currents reduced from the control value of (36.5+/-7.8)% to (26.8+/-4.7) % (n=6, P<0.05). Pirenzepin did not antagonize the inhibition of ACh on I(K) (n=7, P>0.05). Chelerythrine (20 mumol/L) blocked the inhibitory effect of ACh on I(K) and the currents reduced from the control value of (36.5+/-7.8)% to (11.7+/-17.3)% (n=6, P<0.05). On the contrary, PDBu (10 mumol/L) strengthened the inhibition of ACh on I(K) and the drop of currents changed from the control value of (36.5+/-7.8)% to (59.2+/-14.0)% (n=5, P<0.05). PDBu abolished the antagonism of chelerythrine on ACh in cortical neurons. It is suggested that the ACh-induced depolarization of neurons in the cortex is attributed to the inhibition of I(K) that is most likely evoked by the activation of nicotinic ACh receptors and muscarinic M3 receptor via protein kinase C (PKC) signal transduction pathway.

Regulating effects of delayed rectifier potassium channel on the tone of human passively sensitized bronchial smooth muscle / 中国应用生理学杂志

<p><b>AIM</b>To investigate the role of delayed rectifier K+ channel (Kv), Ca2+ -activated K+ channel (K(Ca)) and ATP-sensitive K+ channel (K(ATP)) in the regulation of the resting and contracting tone of human control and passively sensitized bronchial smooth muscle (BSM).</p><p><b>METHODS</b>The regulating effects of the three K+ channels on the tone of human BSM (HBSM) were observed by measuring the isometric tone of bronchial rings in vitro.</p><p><b>RESULTS</b>(1) The contraction of passively sensitized bronchial ring was significantly increased by histamine. (2) Kv blocker 4-aminopyridine (4-AP) caused concentration dependent contraction in resting bronchial rings of two groups, and the contraction sensitivity of the sensitized group rings was significantly stronger than that of control, that is, the negative logarithm of the drug concentration causing 50% of maximal effect (pD2) of the sensitized group rings were significantly larger than that of control rings, but there was no difference in the maximal effect (Emax) of two groups; Kca blocker tetraethylammonium (TEA) and K(ATP) blocker glibenclamide (Glib) had no such effects as those of 4-AP. (3) After pretreatment with 4-AP, the contraction of the control rings could significantly increased by histamine. After 4-AP treatment the Emax was significantly larger than that before 4-AP treatment. But the sensitized group rings had no such change, there was no significant difference in Emax before and after 4-AP treatment.</p><p><b>CONCLUSION</b>(1) Not K(Ca) and K(ATP) but Kv participated in regulation of the resting tone of HBSM. (2) The activity of Kv decreased in bronchial smooth muscle passively sensitized by asthmatic serum compared with that of nonsensitized group. This change might be involved in the mechanism of asthma.</p>

Inhibitory Effects of Norepinephrine on the Potassium Current of Rat Medial Vestibular Nuclear Neurons

BACKGROUND: This study aimed to explore the effects of norepinephrine on the potassium currents of rat medial vestibular nuclear neurons by using the whole-cell patch clamp technique. METHODS: Sprague-Dawley rats aged 14 to 16 days were anesthetized with ether and decapitated. After enzymatic digestion, the portion of the medial vestibular nucleus neurons were obtained by micropunching. The dissociated neurons were transferred into a recording chamber mounted on an inverted microscope and potassium currents were recorded by standard patch-clamp techniques under voltage-clamp modes. RESULTS: Norepinephrine inhibited the whole potassium currents of the medial vestibular nuclear neurons. Outward potassium currents were more suppressed in 4 mM 4-aminopyridine and norepinephrine added solutions than 4 mM 4-aminopyridine only, but were not suppressed in 10 mM tetraethylammonium and norepinephrine added solutions compared to 10 mM tetraethylammonium only. CONCLUSIONS: These results suggest that norepinephrine blocks the delayed rectifier potassium channels in medial vestibular nuclear neurons.

Inhibition of salicylate on potassium channels in rat inferior colliculus neurons / 中华耳鼻咽喉头颈外科杂志

<p><b>OBJECTIVE</b>To understand what role of the transient outward potassium channels and the delayed rectifier potassium channels play in the mechanism of salicylate-induced tinnitus.</p><p><b>METHODS</b>The effects of salicylate on the transient outward potassium channels and the delayed rectifier potassium channels in freshly dissociated inferior colliculus neurons of rats were studied, using the whole-cell voltage clamp method.</p><p><b>RESULTS</b>Salicylate blocked the transient outward potassium current (I(K(A and the delayed rectifier potassium current (I(K(DR in concentration-dependent manner (0.1-1 mmol/L). The IC50 values for the blocking action of salicylate on I(K(A)) and I(K(DR)) were 2.27 and 0.80 mmol/L, respectively. At a concentration of 1 mmol/L, salicylate did not shift the activation and inactivation curves of I(K(A)), but significantly shifted the activation and inactivation curves of I(K(DR)) negatively by approximately 11 mV and 24 mV.</p><p><b>CONCLUSIONS</b>Salicylate inhibits both I(K(A)) and I(K(DR)) in rat inferior colliculus neurons but only significantly affects the activation and inactivation kinetics of I(K(DR)). Effects of I(K(A)) and I(K(DR)), especially I(K(DR)), by salicylate may play an important role in salicylate-induced tinnitus.</p>

Emodin blocks voltage dependent potassium channels in rat proximal colon smooth muscle cells / 药学学报

<p><b>AIM</b>To investigate the effect of emodin on the voltage dependent potassium (K(V)) currents in rat proximal colon smooth muscle cells.</p><p><b>METHODS</b>Whole cell patch clamp technique was used to record potassium currents including fast transient outward current (I(KA)) and delayed rectifier current (I(Kdr)). Contamination of calcium-dependent potassium currents was minimized with CdCl2 in external solution and EGTA in pipette solution.</p><p><b>RESULTS</b>Emodin (1-30 micromol x L(-1)) reversibly and dose-dependently reduced the amplitude of I(Kdr) with an K(d) value of (1.9 +/- 0.1) micromol x L(-1). I(KA) was also inhibited with 30 micromol x L(-1) emodin to a lesser extent. Although acceleration of the decay rate of the K(V) currents was observed, the block by emodin was not through open block mechanism because a steady state level of inhibition of I(Kdr) was achieved during the first pulse from holding potential -70 mV to + 50 mV after the cells were holding at -70 mV for a three minutes interval in the presence of emodin. Emodin (5 micromol x L(-1)) had no effect on the steady-state activation and inactivation kinetics of K(V) currents, but 30 micromol x L(-1) of emodin produced a positive shift of the voltage dependence of activation, and an increase in the steepness of activation gating as well as shifted the voltage dependence of inactivation to positive direction.</p><p><b>CONCLUSION</b>Emodin, not through open block mechanism, markedly reduced the amplitude of I(KA) and I(Kdr) and modulated the gating properties of K(V) channels in a reversible and dose-dependent manner.</p>

Effect of 17beta-estradiol on Kv2.1 current and delayed rectifier potassium current in cultured rat hippocampal neurons / 药学学报

<p><b>AIM</b>To study the effects of 17beta-estradiol on Kv2.1 potassium channel current and delayed rectifier potassium current (IK) in cultured rat hippocampal neurons.</p><p><b>METHODS</b>The effects of 17beta-estradiol on Kv2.1 channel current and IK in cultured rat hippocampal neurons were observed using the whole cell patch clamp techniques.</p><p><b>RESULTS</b>17beta-Estradiol was shown to reduce the amplitude of Kv2.1 current and IK in concentration-dependent manners. The IC50s of 17beta-estradiol blocking Kv2.1 and IK were 2.4 and 4.0 micromol x L(-1), respectively. 17beta-Estradiol (3 micromol x l(-1)) significantly shifted the steady-state activation and inactivation curves of Kv2.1 current to negative potentials. However, it only produced the shift of the steady-state activation curve of IK to the negative potential without effect on the steady-state inactivation of IK.</p><p><b>CONCLUSION</b>17beta-Estradiol inhibits Kv2.1 and IK of hippocampus at similar level. The inhibition of 17beta-estradiol on IK current may be partially via blocking Kv2.1 current.</p>

The effect of ginkgolide B on action potential, L-type calcium current and delayed rectifier potassium current in ischemic guinea pig ventricular myocytes / 中国应用生理学杂志

<p><b>AIM</b>To study the effect of ginkgolide B from Ginkgo leave on action potential (AP), L-type calcium current (I(Ca) - L) and delayed rectifier potassium current (I(K)) in normal and ischemic guinea pig ventricular myocytes.</p><p><b>METHODS</b>With the standard microelectrode technique to record action potential and whole-cell variant patch-clamp technique to record calcium and potassium current.</p><p><b>RESULTS</b>(1) Under normal condition, ginkgolide B shortened APD and had no effect on RP, AP and V(max). Ginkgolide B also increased I(K) in a concentration dependent manner and had no significant effect on I(Ca) - L (2) Under ischemia condition, it was observed that shortening of APD, APA, decrease V(max) and depolarization of RP was induced by ischemia, but ginkgolide B could attenuate above--mentioned changes. (3) Under ischemia condition, I(Ca) - L and I(K) were inhibited, perfusion with ischemia solution containing ginkgolide B could reverse the decrease of I(Ca) - L and I(K).</p><p><b>CONCLUSION</b>Ginkgolide B had protective effect on ischemic myocardium to prevent ischemic arrhythmia.</p>

Effect of corticosterone on the delayed rectified potassium currents of cultured rat hippocampal neurons in vitro / 中国应用生理学杂志

<p><b>AIM</b>The effect of stress hormone corticosterone on hippocampal neurons delayed rectified potassium currents was probed.</p><p><b>METHODS</b>The potassium currents of rat hippocampal neurons in primary culture were measured with patch clamp whole-cell recording.</p><p><b>RESULTS</b>It showed that the amplitudes of the potassium currents in hippocampal neurons decreased. However, the threshold potential of potassium currents increased.</p><p><b>CONCLUSION</b>It is speculated that excessive corticosterone may hurt the hippocampal neurons via its effects on the potassium currents of rat hippocampal cells.</p>

Effects of AlCl3 on transient outward K+ current and delayed rectifier K(+) current in acutely isolated rat hippocampal CA1 neurons / 生理学报

The effects of aluminum chloride (AlCl3) on the transient outward potassium and delayed rectifier K(+) current in hippocampal CA1 neurons of rats were studied by the whole-cell patch clamp technique. It was found that AlCl3 reduced the transient outward potassium current and delayed rectifier K(+) current in a dose-dependent manner. 1000 micromol/L AlCl3 resulted in change in voltage and slope of the half-activation and the half-inactivation of I(A) and I(K). These results imply that AlCl3 may damage potassium channel of the hippocampal CA1 neurons from rats and this may be related to the mechanism of the damage to the central nervous system by aluminum.

Modulation of protein kinase A and protein kinase C on the delayed rectifier potassium current in guinea pig ventricular myocytes / 中国应用生理学杂志

<p><b>AIM</b>To study modulation of protein kinase A (PKA) and protein kinase C (PKC) on the delayed rectifier potassium current (Ik)in guinea pig ventricular myocytes.</p><p><b>METHODS</b>The delayed rectifier potassium current was recorded by using whole cell arrangement of the patch-clamp procedure.</p><p><b>RESULTS</b>cAMP 150 micromol/L increased intracellularly Ik and Ik,tail(pA/pF) from 13.7 +/- 2.1 and 6.1 +/- 0.1 to 18.5 +/- 3.3 and 6.4 +/- 2.1 (P < 0.01, n=6). Ik and Ik,tail(pA/pF) were augmented by 8-CPT-cAMP 150 micromol/L extracellularly from 11.4 +/- 1.8 and 5.3 +/- 0.6 to 17.9 +/- 4.0 and 6.2 +/- 1.3. The half-maximal voltage of activation of Ik was shifted from + 23.3 mV to 18.7 mV by cAMP. Phorbol 12-myristate 13-acetate(PMA, 10.0 micromol/L) applied intracellularly caused an enhance effect on Ik, with increasing Ik and Ik,tail(pA/pF) from 12.9 +/- 1.8 and 5.0 +/- 1.7 to 23.7 +/- 2.8 and 7.5 +/- 1.1. With shifting position potential of depolarization, effect of PMA on Ik was gradually augmented. PMA resulted in shifting the slop of activation curve from +15.3 mV to +25.6 mV, with only a small effect on the half-maximal voltage of activation of Ik.</p><p><b>CONCLUSION</b>Ik was increased by both PKA and PKC, with different characteristics of regulation.</p>

Delayed rectifier K(+) channel regulated by cyclooxygenase-2 in human gastric cancer cell / 中华肿瘤杂志

<p><b>OBJECTIVE</b>To correlate delayed rectifier K(+) channel to cyclooxygenase-2 (COX-2) in onco genesis of human gastric cancer cell.</p><p><b>METHODS</b>Human COX-2 encoding gene was cloned with RT-PCR strategy and its antisense recombinant eukaryotic expression vector was constructed. COX-2 highly expressed human gastric cancer cell line SGC7901 was stably transfected with the antisense vector. The whole-cell recording technique of perforated patch clamp was employed to observe the change of delayed rectifier K(+) current (I(k)) of SGC7901 after gene transfer or treatment with COX-2 inhibitor indomethacin. MTT was also performed to determine the effect of delayed rectifier K(+) channel inhibitors on cell growth.</p><p><b>RESULTS</b>Stably transfected cell (7901-AS) was obtained and a down-regulated expression of COX-2 protein and mRNA in the cell was achieved. Patch clamp recording showed that both SGC7901 and 7901-AS cells had a typical delayed rectifier K(+) current. However, I(k) was significantly lower (P < 0.01) in transfected cell or cell treated with indomethacin at each test potential. The altered I(k) could be entirely recovered after drug removal from the cells. K(+) channel blockers tetraethylammonium (TEA) and 4-aminopyridine (4-AP) could retard the growth of SGC7901 and the transfected cell in a dose-dependent manner.</p><p><b>CONCLUSION</b>Delayed rectifier K(+) channel, existing in human gastric cancer cell line SGC7901, is related to the growth of the cell. The highly expressed COX-2 may affect the biological behavior of gastric cancer cell by regulating this ion channel.</p>

Effects of chronic exposure to beta-amyloid-peptide25-35 on the mRNA expressions of voltage-gated outward potassium channel subunits in cultured rat hippocampal neurons / 药学学报

<p><b>AIM</b>To investigate mRNA expression changes of voltage-gated outward potassium channel subtypes in cultured rat hippocampal neurons after chronic exposure to beta-amyloid-petitde25-35 (beta-AP25-35).</p><p><b>METHODS</b>mRNA expression was detected by RT-PCR, comparative expression levels were determined by imaging densitometer.</p><p><b>RESULTS</b>Delayed rectifying (Kv2.1, Kv1.5), transient outward (Kv1.4, Kv4.2) and large conductance calcium-activated (rSlo) potassium channel mRNA were expressed in cultured rat hippocampal. In the presence of beta-AP25-35 3 mumol.L-1 for 24 h, the relative expression level of Kv2.1 was significantly increased (n = 3, P < 0.05); the other subtypes were not changed obviously (n = 3, P > 0.05). The increase of Kv2.1 mRNA mainly happened between 24 and 36 h after exposure to beta-AP25-35. After exposure to beta-AP25-35 for 60 h, Kv2.1 mRNA decreased significantly (n = 3, P < 0.01).</p><p><b>CONCLUSION</b>The upregulation of Kv2.1 on transcription levels may be involved in the enhancement of delayed rectifying outward potassium (Ik) current induced by beta-AP25-35.</p>