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PubMed1992

The cardiotonic bipyridine AWD 122-60 inhibits adenosine triphosphate-sensitive potassium channels of mouse skeletal muscle.

The inhibition of ATP-sensitive potassium channels in mouse skeletal muscle by the cardiotonic bipyridine AWD 122-60 was investigated with the patch-clamp technique. In excised patches of the inside-out configuration, internally applied AWD 122-60 (10(-6)-10(-3) mol/l) reversibly reduced the open-probability of single ATP-sensitive potassium channels. The agent shortened the periods of channel activity but did not affect the channel conductance. At positive membrane potentials channel inhibition by AWD 122-60 was more pronounced than at negative potentials, the drug concentrations producing 50% channel inhibition were 11 mumol/l at +40 mV and 29 mumol/l at -40 mV. The Hill coefficients of the concentration-response curves were in the range between 0.5 and 0.6 for both potentials. Internal application of another cardiotonic bipyridine, milrinone (10(-4) mol/l), had no effects on ATP-sensitive potassium channels in skeletal muscle. Possible effects of the inhibition of ATP-sensitive potassium channels in heart muscle by AWD 122-60 are discussed.

Adenosine Triphosphate↗
PubMed2002

Activation of mitochondrial ATP-dependent potassium channels protects neurons against ischemia-induced death by a mechanism involving suppression of Bax translocation and cytochrome c release.

Neurons express a variety of plasma-membrane potassium channels that play important roles in regulating neuronal excitability and synaptic transmission, but also contain mitochondrial ATP-sensitive potassium channels, the functions of which are unknown. Studies of cardiac cells suggest that similar mitochondrial ATP-sensitive potassium channels are involved in the process of ischemic preconditioning, suggesting a role in regulating cell survival. The authors report that mice given diazoxide, an activator of mitochondrial ATP-sensitive potassium channels, exhibited a large (60% to 70%) decrease in cortical infarct size after permanent occlusion of the middle cerebral artery. Diazoxide decreases neuronal apoptosis and increases astrocyte survival and activation in the penumbral region of the ischemic cortex. The neuroprotective effect of diazoxide is abolished by 5-hydroxydecanoate, a selective antagonist of mitochondrial ATP-sensitive potassium channels. Studies of cultured hippocampal neurons reveal that diazoxide depolarizes mitochondria, prevents cytochrome c release, and protects cells against death induced by staurosporine and chemical hypoxia. Diazoxide increased the levels of Bcl2 and inhibited the association of Bax with mitochondria in neurons exposed to an apoptotic insult, suggesting that activation of mitochondrial ATP-sensitive potassium channels may stabilize mitochondrial function by differentially modulating proapoptotic and antiapoptotic proteins. Collectively, the data suggest that mitochondrial ATP-sensitive potassium channels play a key role in modulating neuronal survival under ischemic conditions, and identify agents that activate mitochondrial ATP-sensitive potassium channels as potential therapeutics for stroke and related neurodegenerative conditions.

Animals↗
PubMed1996

Molecular determinants for activation and inactivation of HERG, a human inward rectifier potassium channel.

1. The human eag-related potassium channel, HERG, gives rise to inwardly rectifying K+ currents when expressed in Xenopus oocytes. 2. The apparent inward rectification is caused by rapid inactivation. In extracellular Cs+ solutions, large outward currents can be recorded having an inactivation time constant at 0 mV of about 50 ms with an e-fold change every 37 mV. 3. HERG channel inactivation is not caused by an amino-terminal ball structure, as a deletion of the cytoplasmic amino terminus (HERG delta 2-373) did not eliminate inactivation. However, channel deactivation was accelerated about 12-fold at -80 mV. 4. Mutation of S631 to A, the homologous residue of eag channels, in the outer mouth of the HERG pore completely abolished channel inactivation. 5. Activity of HERG channels depended on extracellular cations, which are effective for channel activation, in the order Cs+ > K+ > > Li+ > Na+. The point mutation S631A strongly reduced this channel regulation. 6. By analogy to functional aspects of cloned voltage-gated potassium channels, rectification of HERG, as well as its kinetic properties during the course of an action potential, are presumably governed by a mechanism reminiscent of C-type inactivation.

Alanine↗
PubMed1996

Eight potassium channel families revealed by the C. elegans genome project.

The wealth of accumulating data from the Caenorhabditis elegans genome sequencing project has rapidly accelerated the discovery of novel potassium channel genes and now places within reach the possibility of describing the total complement of potassium channels used by an individual species. Using annotated GenBank sequences, BLAST searches of unfinished sequences and degenerate oligonucleotide polymerase chain reaction (PCR) screens, we have identified and compiled genes for 38 C. elegans potassium channel and two cyclic nucleotide-gated cation channel subunits, representing eight conserved multigene families. Novel families of potassium channel genes were revealed, as well as conserved homologues of all known vertebrate families. Two separate families represent C. elegans homologues for human potassium channels recently implicated in hereditary long QT arrhythmias. Of particular note is an exceptionally large class of at least 23 genes with a novel subunit structure having two tandem 'P' domains; these channels may form as dimers in contrast to all other potassium channel types which form as tetramers. The 40 potassium channel genes are evenly distributed on all six C. elegans chromosomes, with the exception of the instances of gene clustering on the fifth and X chromosomes.

Amino Acid Sequence↗
PubMed1997

ATP-dependent potassium channel from rat liver mitochondria: inhibitory analysis, channel clusterization.

An inhibitor of potassium mitochondrial channels quinidine (0.1 mM) closed the ATP-sensitive potassium channels isolated from mitochondria and reconstituted into a bilayer lipid membrane. Inhibitors of cytoplasm membrane K-channels (ouabain, tetraethyl ammonium, and cesium ions) produced no effect on the ATP-sensitive mitochondria K-channels; 0.5-2 microM glybenclamide did not affect the reconstituted channels, either. The multiplicity of jumps of conductivity at small concentration of the protein and the maintenance of ion selectivity at switching various levels of conductivity lead us to assume that the large channels are clusters of elementary channels. The average frequency of channel-cluster switchovers between various levels of conductivity is much higher than at the elementary channel.

Adenosine Triphosphate↗
PubMed1993

Activation and inactivation of the bursting potassium channel from fused Torpedo synaptosomes.

1. The voltage dependence of the bursting potassium channel in fused synaptosomes from Torpedo electric organ was studied in vitro, using the inside-out and the cell-attached configurations of the patch clamp technique. 2. The patch of membrane was held at various holding potentials (-140 to -50 mV) and then stepped to test potentials (-50 to +40 mV) for periods ranging from 5 to 300 ms. Each potential step was repeated 200-600 times. After subtraction of the capacitative transients and the leakage currents, an ensemble-averaged current was obtained. This ensemble current showed a marked activation upon depolarization, followed by an inactivation. 3. The activation of the bursting potassium channel is markedly dependent on the voltage step. Activation was detected at voltages positive to -50 mV. The peak of the ensemble current increases with the degree of depolarization, while the time to the peak decreases. With progressively larger depolarization, there is a shortening in the delay between the onset of the voltage step and the opening of the bursting potassium channels. 4. The inactivation phase of the ensemble current could be described adequately in most of the experiments, as a single exponential decay to a steady-state inactivation level. The time constant of inactivation was not markedly voltage dependent. 5. Single channel analysis of the inactivation reveals that it is due to a reduction in the number of channel openings and not due to changes in single channel current amplitude or channel mean open time along the pulse. 6. The holding potential has a marked effect on the peak amplitude of the ensemble current, indicating that hyperpolarization removes inactivation and depolarization induces it. The peak amplitude vs. voltage relation was fitted by the Boltzmann equation. The half-maximal inactivation was -105.2 +/- 5.8 mV (mean +/- S.E.M.), suggesting that at the resting potential a substantial fraction of the bursting potassium channels is in an inactivated state. 7. Two-pulse experiments show that the recovery from inactivation is a slow process which lasts well over 1 s. 8. High-frequency stimulation (20-66.7 Hz) by 5 ms pulses produces a progressive decline in the peak ensemble current amplitude. The decline is larger at higher stimulation frequencies.(ABSTRACT TRUNCATED AT 400 WORDS)

4-Aminopyridine↗
PubMed2006

The role of potassium channels in the vasodilatory effect of levosimendan in human internal thoracic arteries.

OBJECTIVE: We investigated the role of potassium channels in vasodilatory effect of levosimendan in human internal thoracic arteries. METHODS: Samples of redundant internal thoracic arteries obtained from patients undergoing a coronary artery bypass graft surgery were cut into 3 mm wide rings and suspended in 20 ml organ baths. Isometric tension was continuously measured with an isometric force transducer connected to a computer-based data acquisition system. RESULTS: Levosimendan (10(-8)-10(-5) M) or cromakalim (10(-8)-10(-5) M) produced concentration-dependent relaxation responses in human internal thoracic arteries precontracted by 10(-6) M phenylephrine. The relaxant responses to levosimendan did not differ significantly between endothelium-intact and endothelium-denuded preparations. Incubation of human internal thoracic artery rings with adenosine 3',5'-triphosphate (ATP)-dependent potassium channel blocker glibenclamide (10(-6) M) for 30 min significantly inhibited the relaxant responses to both levosimendan and cromakalim. The Ca2+-activated potassium channel blocker iberiotoxin (10(-7) M) also caused a significant but smaller inhibition on relaxant responses to levosimendan. Incubation of the rings with the voltage-dependent potassium channel blocker 4-aminopyridine (5 mM) for 10 min did not cause significant alterations in relaxant responses to levosimendan. CONCLUSIONS: The findings of this study suggested that levosimendan-induced relaxation responses in human internal thoracic arteries were depended on the activation of ATP-dependent and Ca2+-activated potassium channels.

Aged↗
PubMed2003

Biophysical characteristics of a new mutation on the KCNQ1 potassium channel (L251P) causing long QT syndrome.

The congenital long QT syndrome (LQTS) is a hereditary cardiac disease characterized by prolonged ventricular repolarization, syncope, and sudden death. Mutations causing LQTS have been identified in various genes that encode for ionic channels or their regulatory subunits. Several of these mutations have been reported on the KCNQ1 gene encoding for a potassium channel or its regulatory subunit (KCNE1). In this study, we report the biophysical characteristics of a new mutation (L251P) in the transmembrane segment 5 (S5) of the KCNQ1 potassium channel. Potassium currents were recorded from CHO cells transfected with either wild type or mutant KCNQ1 in the presence or in the absence of its regulatory subunit (KCNE1), using the whole-cell configuration of the patch clamp technique. Wild-type KCNQ1 current amplitudes are increased particularly by KCNE1 co-expression but no current is observed with the KCNQ1 (L251P) mutant either in the presence or in the absence of KCNE1. Coexpressing KCNE1 with equal amount of cDNAs encoding wild type and mutant KCNQ1 results in an 11-fold reduction in the amplitude of potassium currents. The kinetics of activation and inactivation and the activation curve are minimally affected by this mutation. Our results suggest that the dominant negative effect of the P251L mutation on KCNQ1 channel explains the prolonged repolarization in patients carrying this mutation.

Adolescent↗
PubMed2003

[Changes of potassium channel activity of hindlimb arterial smooth muscle cells in tail-suspended rats].

OBJECTIVE: To examine the change of potassium channel function in hindlimb arterial smooth muscle cells in tail-suspended rats and to elucidate the underlying electro-physiological mechanisms responsible for the depressed vascular responsiveness of hindlimb arteries induced by simulated weightlessness. METHOD: The contractile responsiveness of femoral arterial rings of 1-wk and 4-wk tail-suspended rats to potassium channel blockers, tetraethylammonium chloride (TEA) and 4-aminopyridine (4-AP), were recorded, and the currents of large conductance calcium-dependent potassium channel (BK(Ca)) and voltage activated potassium channel (Kv) of vascular smooth muscle cells (VSMCs) in saphenous arteries from 1-wk tail-suspended rats were recorded using the whole cell recording mode of patch clamp technique. RESULT: The femoral arteries from of 1-wk and 4-wk tail-suspended rats showed a decreased contractile response to 60 mM KCl, and the ratio of their contractile responses induced by TEA or 4-AP to their responses induced by 60 mM KCl increased significantly after 1-wk and 4-wk simulated weightlessness. However no difference was found between 1-wk and 4-wk tail-suspended rats. The whole cell current recording showed that BK(Ca) current densities and K(v) current densities of VSMCs in saphenous artery increased significantly after 1-wk simulated weightlessness. CONCLUSION: The contractile response of hindlimb arteries to KCl decreased after simulated weightlessness. The activities of BK(Ca) and K(v) of smooth muscle cells in hindlimb arteries from tail-suspended rats increased, and these changes might be among the electro-physiological mechanisms involved in the depressed vasoreactivity of hindlimb arteries due to simulated weightlessness.

4-Aminopyridine↗
PubMed2005

Activation of mitochondrial ATP-sensitive potassium channels improves rotenone-related motor and neurochemical alterations in rats.

Our previous studies revealed that activation of mitochondrial ATP-sensitive potassium channels exerted protective effects on rotenone-treated rats and cultured cells. The aim of the present study is to examine the potential therapeutic effects of iptakalim, an ATP-sensitive potassium-channel opener, and diazoxide, a selective mitochondrial ATP-sensitive potassium-channel opener, on Parkinsonian symptoms in rats induced by rotenone. Rats were treated with rotenone (2.5 mg/kg s.c.) daily for 4 wk. This treatment caused a depletion of dopamine in the striatum and substantia nigra. Behaviourally, rotenone-infused rats exhibit Parkinsonian symptoms. Catalepsy was estimated by a 9-cm bar test. Treatment with L-dopa (10 mg/kg.d p.o.), iptakalim (0.75, 1.5, 3.0 mg/kg.d p.o.) and diazoxide (3.0 mg/kg.d p.o.) for 2 wk improved behavioural dysfunction and elevated dopamine contents in the striatum and substantia nigra of rotenone-treated rats. Studies also found that iptakalim and diazoxide could reduce the enzymic activities and mRNA levels of inducible nitric oxide synthase elicited by chronic administration of rotenone. All neurorestorative effects by both iptakalim and diazoxide were abolished by 5-hydroxydecanoate, a selective mitochondrial ATP-sensitive potassium-channel blocker. Collectively, the data suggested that mitochondrial ATP-sensitive potassium channels play a key role in improving both Parkinsonian symptoms and neurochemistry alterations of rotenone model rats, and selective activation of mitochondrial ATP-sensitive potassium channels may provide a new therapeutic strategy for treatment of early Parkinson's disease.

Animals↗
PubMed2006

Protein distribution of Kcnq1, Kcnh2, and Kcne3 potassium channel subunits during mouse embryonic development.

Voltage-dependent potassium channels consist of a pore-forming alpha-subunit, which is modulated by additional beta-ancillary or regulatory subunits. Kcnq1 and Kcnh2 alpha-channel subunits play pivotal roles in the developing and adult heart. However, Kcnq1 and Kcnh2 have a much wider expression profile than strictly confined to the myocardium, similar to their putative regulatory Kcne1-5 beta-subunits. At present, the distribution of distinct potassium channel subunits has been partially mapped in adult tissues, whereas almost no information is available during embryonic development. In this study, we report a detailed analysis of Kcnq1, Kcnh2, and Kcne3 protein expression during mouse embryogenesis. Our results demonstrate that Kcnq1 and Kcnh2 are widely distributed. Coexpression of both alpha-subunits is observed in a wide variety of organs, such as heart and the skeletal muscle, whereas others display unique Kcnq1 or Knch2 expression. Interestingly, Kcne3 expression is also widely observed in distinct tissue layers during embryogenesis, supporting the notion that an exquisite balance of alpha- and beta-subunit expression is required for modulating potassium conductance in distinct organs and tissue layers.

Animals↗
PubMed1990

Three different potassium channels in human atrium. Contribution to the basal potassium conductance.

We applied the cell-attached and inside-out patch-clamp technique under symmetrical isotonic potassium conditions on single human (and guinea pig) atrial cells. The human cells were isolated by a modified method to that described earlier. Our aim was twofold: 1) to study the single-channel characteristics of potassium channels in human atrial single cells, present under basal conditions (iK1 and iK(ATP] or when stimulated with 10(-5) M acetylcholine; and 2) to calculate the contribution of these three channel types to the total basal potassium conductance in human atrial cells, and to compare the results with data on guinea pig atrial cells under the same conditions. We found that in human cells 58% of the patches (n = 42/74) contained acetylcholine-sensitive potassium channels: their conductance was 42 +/- 1.2 pS and mean open time (tau o) was 1.7 +/- 0.5 msec. They showed sporadic openings in the absence of agonist, and activation by acetylcholine was G-protein dependent. In 16% of the patches (n = 7/44), adenosine (10(-4) M) activated the same channels, but the activity was lower than when stimulated by acetylcholine. In 18% of the patches (n = 9/51), an iK1 channel was present (conductance, 27 pS; tau o, 8.7 msec), whereas in the cell-attached mode, ATP-dependent channels were never seen. However, they were present in half of the inside-out patches on washout of ATPi (conductance, 73 pS; tau o, 1.4 msec). The basal potassium conductance (i.e., in the absence of any exogenous hormone or neurotransmitter) was mainly due to iK1 channels in both human and guinea pig cells, a finding that is in contrast with previous reports. However, the potassium current that is induced by acetylcholine is much higher in guinea pig than in human isolated cells; a fraction of it would suffice to fully determine the resting potassium conductance in guinea pig atrial cells, whereas it can play only a modulatory role in human cells. This difference could be important in species-specific autonomic modulation and antiarrhythmic drug action.

Acetylcholine↗
PubMed1996

Mechanism of action of the epileptogenic drug pentylenetetrazol on a cloned neuronal potassium channel.

The action of the epileptogenic agent pentylenetetrazol (PTZ) on a cloned potassium channel of the rat brain was studied. The Kv1.1 channel was expressed in oocytes of Xenopus laevis and potassium currents were investigated in outside-out and inside-out membrane patches. The results show that PTZ increased the multi-channel potassium currents at strongly negative potentials and decreased them at potentials positive to -35 mV both in outside-out and inside-out membrane patches. The extent and manner of PTZ action, the concentration dependence as well as the onset and time course of the PTZ effect were the same both in outside-out and inside-out membrane patches. The single-channel potassium currents showed an increase in open probability and frequency of opening and a decrease in close time at -50 mV and vice versa at 0 mV with application of PTZ. The amplitude of single-channel current, the open time and the latency to the first channel opening remained almost unchanged under PTZ. The results indicate that PTZ acts via the cell membrane and influences the membrane-associated part of the potassium channel. Thereby, PTZ accelerates the transition from the inactivated to the open state of the channel at strongly negative potentials and reduces it at slightly negative and positive potentials. This mechanism may be the basis for a gate function which is in favour of the development of epileptic discharges.

Animals↗
PubMed2004

Effect of chronic cigarette smoking on large-conductance calcium-activated potassium channel and Kv1.5 expression in bronchial smooth muscle cells of rats.

To investigate the role of potassium channels in the pathogenesis of airway hyperresponsiveness induced by cigarette smoking, the alteration in expression of large-conductance calcium-activated potassium channel (BKca) and voltage-dependent delayed rectifier potassium channel (Kv1.5) in bronchial smooth muscle cells were investigated in chronic cigarette smoking rats. Airway responsiveness was determined, hematoxylin and eosin staining, immuno-histochemistry, in-situ hybridization and western blot techniques were used. The results showed: (1) Chronic cigarette smoking down-regulated the protein synthesis and mRNA expression of BKca and Kv1.5 in bronchial and bronchiolar smooth muscles. (2) BKca decreased more markedly than Kv1.5 in bronchi, but there was no difference between them in bronchioli. (3) No changes in the expression of these two potassium channel proteins were found in extracted cell membrane protein from lung tissue. The results suggest that chronic cigarette smoking can down-regulate the levels of BKca and Kv1.5 in rat bronchial smooth muscle cells in vivo, which might contribute to the mechanism of airway hyperresponsiveness induced by cigarette smoking.

Animals↗
PubMed1996

Is potassium channel opening an effective form of preconditioning before cardioplegia?

BACKGROUND: Opening of adenosine triphosphate-sensitive potassium channels might be one of the mechanisms by which preconditioning preserves the myocardium against ischemic damage. The present study was therefore designed to compare the protective efficacy of ischemic preconditioning with that of pharmacologic preconditioning involving the use of a potassium channel opener in a surgically relevant model of cold cardioplegic arrest. METHODS: Thirty isolated isovolumic rat hearts were subjected to 2 hours of potassium arrest at an average myocardial temperature of 23 degrees C, followed by 1 hour of reperfusion. Three groups (n = 10 per group) were studied: (1) control (no prearrest intervention); (2) ischemic preconditioning, achieved with 5 minutes of noflow ischemia followed by 5 minutes of reperfusion before arrest; and (3) pharmacologic preconditioning, achieved with a 5-minute infusion of the potassium channel opener nicorandil (10 mumol/L) followed by 5 minutes of drug-free perfusion before arrest. Standard functional indices were measured at multiple times during reperfusion, at the end of which pressure-volume curves were constructed and compared with those obtained at baseline. RESULTS: Both ischemically and pharmacologically preconditioned hearts recovered systolic and diastolic function to a significantly greater extent than the controls. There was no difference in the recovery patterns between the forms of preconditioning. However, analysis of the postischemic pressure-volume curves demonstrated that nicorandil-preconditioned hearts incurred the smallest losses of compliance throughout the ischemia-reperfusion sequence. CONCLUSIONS: The protective effects of a standard ischemic preconditioning challenge on functional recovery after an episode of moderately hypothermic cardioplegic arrest can be duplicated by pharmacologic opening of adenosine triphosphate-sensitive potassium channels. This finding may be of clinical relevance because of the availability of potassium channel openers, such as nicorandil, for human use.

Analysis of Variance↗
PubMed1989

Potassium channels in chick lens epithelium change with maturation.

Before hatching, chick embryos show a high incidence of inwardly rectifying potassium channels and calcium-activated potassium channels in the apical membrane of their lens epithelium. Subsequent to hatching, these channel types disappear while, at about the same time, a new calcium insensitive maxi potassium channel appears. This new channel shows several properties in common with the calcium-activated maxi potassium channels but is different in its conductive and gating properties.

Analog-Digital Conversion↗
PubMed1999

Molecular and functional characterization of s-KCNQ1 potassium channel from rectal gland of Squalus acanthias.

Functional and pharmacological data point to the involvement of KCNQ1/IsK potassium channels in the basolateral potassium conductance of secretory epithelia. In this study, we report the cloning and electrophysiological characterization of the KCNQ1 protein from the salt secretory rectal gland of the spiny dogfish (Squalus acanthias). The S. acanthias KCNQ1 (s-KCNQ1) cDNA was cloned by polymerase chain reaction (PCR) intensive techniques and showed overall sequence similarities with the KCNQ1 potassium channel subunits of Man, mouse and Xenopus laevis of 64, 70 and 77%, respectively, at the translated amino acid level. Analysis of s-KCNQ1 expression on a Northern blot containing RNA from heart, rectal gland, kidney, brain, intestine, testis, liver and gills revealed distinct expression of 7.4-kb s-KCNQ1 transcripts only in rectal gland and heart. Voltage-clamp analysis of s-KCNQ1 expressed in Xenopus oocytes showed pronounced electrophysiological similarities to human and murine KCNQ1 isoforms, with a comparable sensitivity to inhibition by the chromanol 293B. Coexpression of s-KCNQ1 with human-IsK (h-IsK) induced currents with faster activation kinetics and stronger rectification than observed after coexpression of human KCNQ1 with h-IsK, with the voltage threshold of activation shifted to more negative potentials. The low activation threshold at approximately -60 mV in combination with the high expression in rectal gland cells make s-KCNQ1 a potential candidate responsible for the basolateral potassium conductance.

Animals↗
PubMed1998

Auxiliary subunits of Shaker-type potassium channels.

Voltage-gated potassium channels are important determinants of membrane excitability. This family of ion channels is composed of several classes of proteins, including the pore-forming Kvalpha subunits and the recently identified auxiliary Kvbeta subunits. A combination of a large number of genes that encode various alpha subunits and beta subunits and the selective formation of alpha-alpha and alpha-beta heteromultimeric channels provides rich molecular diversity that allows for regulated functional heterogeneity in both excitable tissues and nonexcitable tissues. Because the Kvbeta subunits can either upregulate or downregulate potassium currents, depending on the specific subunit combination, it is essential to understand their function at the molecular level. Furthermore, targeted changes of the Kvbeta expression or disruption of certain alpha-beta interactions could serve as a molecular basis for designing drugs and therapy to regulate excitability clinically.

Journal Article↗