Potassium Channel Function
Published by Hoozhooz on 2007/9/27 (4250 reads)
: Curr Pharm Des. 2006;12(18):2271-83.
The cardiac hERG/IKr potassium channel as pharmacological target: structure, function, regulation, and clinical applications.
Thomas D, Karle CA, Kiehn J.
Department of Cardiology, Medical University Hospital Heidelberg, Im Neuenheimer Feld 410, D-69120 Heidelberg, Germany.
Human ether-a-go-go-related gene (hERG) potassium channels conduct the rapid component of the delayed rectifier potassium current, IKr, which is crucial for repolarization of cardiac action potentials. Moderate hERG blockade may produce a beneficial class III antiarrhythmic effect. In contrast, a reduction in hERG currents due to either genetic defects or adverse drug effects can lead to hereditary or acquired long QT syndromes characterized by action potential prolongation, lengthening of the QT interval on the surface ECG, and an increased risk for "torsade de pointes" arrhythmias and sudden death. This undesirable side effect of non-antiarrhythmic compounds has prompted the withdrawal of several blockbuster drugs from the market. Studies on mechanisms of hERG channel inhibition provide significant insights into the molecular factors that determine state-, voltage-, and use-dependency of hERG current block. In addition, crucial properties of the high-affinity drug binding site in hERG and its interaction with drug molecules have been identified, providing the basis for more refined approaches in drug design, safety pharmacology and in silico modeling. Recently, mutations in hERG have been shown to cause current increase and hereditary short QT syndrome with a high risk for life-threatening arrhythmias. Finally, the discovery of adrenergic mechanisms of hERG channel regulation as well as the development of strategies to enhance hERG currents and to modify intracellular hERG protein processing may provide novel antiarrhythmic options in repolarization disorders. In conclusion, the increasing understanding of hERG channel function and molecular mechanisms of hERG current regulation could improve prevention and treatment of hERG-associated cardiac repolarization disorders.
Publication Types:
Research Support, Non-U.S. Gov't
Review
PMID: 16787254 [PubMed - indexed for MEDLINE]
--------------------------------------------------------------------------------
2: Physiology (Bethesda). 2005 Dec;20:408-16.
The KCNQ1 potassium channel: from gene to physiological function.
Jespersen T, Grunnet M, Olesen SP.
Department of Medical Physiology, University of Copenhagen, Denmark.
The voltage-gated KCNQ1 (KvLQT1, Kv7.1) potassium channel plays a crucial role in shaping the cardiac action potential as well as in controlling the water and salt homeostasis in several epithelial tissues. KCNQ1 channels in these tissues are tightly regulated by auxiliary proteins and accessory factors, capable of modulating the properties of the channel complexes. This paper reviews the current knowledge about the KCNQ1 channel with a major focus on interacting proteins and physiological functions.
Publication Types:
Research Support, Non-U.S. Gov't
Review
PMID: 16287990 [PubMed - indexed for MEDLINE]
--------------------------------------------------------------------------------
3: Biochim Biophys Acta. 2003 Sep 30;1606(1-3):1-21.
Mitochondrial potassium transport: the role of the mitochondrial ATP-sensitive K(+) channel in cardiac function and cardioprotection.
Garlid KD, Dos Santos P, Xie ZJ, Costa AD, Paucek P.
Department of Biology, Portland State University, 1719 SW 10th Avenue, PO Box 751, Portland, OR 97207, USA. garlid@pdx.edu
Coronary artery disease and its sequelae-ischemia, myocardial infarction, and heart failure-are leading causes of morbidity and mortality in man. Considerable effort has been devoted toward improving functional recovery and reducing the extent of infarction after ischemic episodes. As a step in this direction, it was found that the heart was significantly protected against ischemia-reperfusion injury if it was first preconditioned by brief ischemia or by administering a potassium channel opener. Both of these preconditioning strategies were found to require opening of a K(ATP) channel, and in 1997 we showed that this pivotal role was mediated by the mitochondrial ATP-sensitive K(+) channel (mitoK(ATP)). This paper will review the evidence showing that opening mitoK(ATP) is cardioprotective against ischemia-reperfusion injury and, moreover, that mitoK(ATP) plays this role during all three phases of the natural history of ischemia-reperfusion injury preconditioning, ischemia, and reperfusion. We discuss two distinct mechanisms by which mitoK(ATP) opening protects the heart-increased mitochondrial production of reactive oxygen species (ROS) during the preconditioning phase and regulation of intermembrane space (IMS) volume during the ischemic and reperfusion phases. It is likely that cardioprotection by ischemic preconditioning (IPC) and K(ATP) channel openers (KCOs) arises from utilization of normal physiological processes. Accordingly, we summarize the results of new studies that focus on the role of mitoK(ATP) in normal cardiomyocyte physiology. Here, we observe the same two mechanisms at work. In low-energy states, mitoK(ATP) opening triggers increased mitochondrial ROS production, thereby amplifying a cell signaling pathway leading to gene transcription and cell growth. In high-energy states, mitoK(ATP) opening prevents the matrix contraction that would otherwise occur during high rates of electron transport. MitoK(ATP)-mediated volume regulation, in turn, prevents disruption of the structure-function of the IMS and facilitates efficient energy transfers between mitochondria and myofibrillar ATPases.
Publication Types:
Research Support, Non-U.S. Gov't
Research Support, U.S. Gov't, P.H.S.
Review
PMID: 14507424 [PubMed - indexed for MEDLINE]
--------------------------------------------------------------------------------
4: Am J Physiol Lung Cell Mol Physiol. 2003 May;284(5):L689-700.
Chloride and potassium channel function in alveolar epithelial cells.
O'Grady SM, Lee SY.
Department of Physiology, University of Minnesota, St. Paul, Minnesota 55108, USA. ograd001@umn.edu
Electrolyte transport across the adult alveolar epithelium plays an important role in maintaining a thin fluid layer along the apical surface of the alveolus that facilitates gas exchange across the epithelium. Most of the work published on the transport properties of alveolar epithelial cells has focused on the mechanisms and regulation of Na(+) transport and, in particular, the role of amiloride-sensitive Na(+) channels in the apical membrane and the Na(+)-K(+)-ATPase located in the basolateral membrane. Less is known about the identity and role of Cl(-) and K(+) channels in alveolar epithelial cells, but studies are revealing important functions for these channels in regulation of alveolar fluid volume and ionic composition. The purpose of this review is to examine previous work published on Cl(-) and K(+) channels in alveolar epithelial cells and to discuss the conclusions and speculations regarding their role in alveolar cell transport function.
Publication Types:
Review
PMID: 12676759 [PubMed - indexed for MEDLINE]
--------------------------------------------------------------------------------
5: Clin Exp Pharmacol Physiol. 2002 Apr;29(4):305-11.
Oxidative stress and potassium channel function.
Liu Y, Gutterman DD.
Cardiovascular Center, Medical College of Wisconsin, Milwaukee, Wisconsin 53226, USA. ypliu@mcw.edu
1. Modulation of K+ channel activities by cellular oxidative stress has emerged as a significant determinant of vasomotor function in multiple disease states. 2. Evidence from in vitro and in vivo studies suggest that superoxide (O2-) and hydrogen peroxide (H2O2) enhance BKCa channel activity in rat and cat cerebral arterioles; however, activity is decreased by peroxynitrite (ONOO-) in rat cerebral arteries. The mechanisms of changes in BKCa channel properties are not fully understood and may involve oxidation of cysteine residues that are located in the cell membranes. 3. Studies further suggest that O2- increases KATP channel activity in guinea-pig cardiac myocytes, but decreases opening in cerebral vasculature. Both H2O2 and ONOO- enhance KATP channel activity in the myocardium and in coronary, renal, mesenteric and cerebral vascular beds. Alteration of KATP channels by free radicals may be due to oxidation of SH groups or changes in the cytosolic concentration of ATP. 4. It does appear that O2- produced by either reaction of xanthine and xanthine oxidase or elevated levels of glucose reduces Kv channel activity and the impairments can be partially restored by free radical scavengers, superoxide dismutase and catalase. 5. Thus, redox modulation of potassium channel activity is an important mechanism regulating cell vascular smooth muscle membrane potential.
Publication Types:
Review
PMID: 11985541 [PubMed - indexed for MEDLINE]
--------------------------------------------------------------------------------
6: Arterioscler Thromb Vasc Biol. 2001 Jan;21(1):28-38.
Potassium channel function in vascular disease.
Sobey CG.
Department of Pharmacology, The University of Melbourne, Parkville, Victoria, Australia. cg.sobey@unimelb.edu.au
Potassium ion (K(+)) channel activity is a major regulator of vascular muscle cell membrane potential (E(m)) and is therefore an important determinant of vascular tone. There is growing evidence that the function of several types of vascular K(+) channels is altered during major cardiovascular diseases, such as chronic hypertension, diabetes, and atherosclerosis. Vasoconstriction and the compromised ability of an artery to dilate are likely consequences of defective K(+) channel function in blood vessels during these disease states. In some instances, increased K(+) channel function may help to compensate for increased vascular tone. Endothelial cell dysfunction is commonly associated with cardiovascular disease, and altered activity of nitric oxide, prostacyclin, and endothelium-derived hyperpolarizing factor could also contribute to changes in resting K(+) channel activity, E(m), and K(+) channel-mediated vasodilatation. Our current knowledge of the effects of disease on vascular K(+) channel function almost exclusively relies on interpretation of data obtained by using pharmacological modulators of K(+) channels. As further progress is made in the development of more selective drugs and through molecular approaches such as gene targeting technology in mice, specific K(+) channel abnormalities and their causes in particular diseases should be more readily identified, providing novel directions for vascular therapy.
Publication Types:
Research Support, Non-U.S. Gov't
Review
PMID: 11145930 [PubMed - indexed for MEDLINE]
--------------------------------------------------------------------------------
7: Postepy Hig Med Dosw. 2000;54(3):381-90.
[Regulation of potassium channel function in T lymphocytes by intracellular second messengers for calcium, cyclic AMP and membrane lipid metabolites]
[Article in Polish]
Teisseyre A.
Katedra i Zakład Biofizyki Akademii Medycznej we Wrocławiu.
This review focuses on the influence of well-known intracellular second messengers on the activity of potassium channels expressed in human T lymphocytes. Basic biophysical properties of the channels are briefly presented. Available data on the regulatory role of intracellular calcium and cyclic AMP is reviewed. Finally, a possible influence of lipid compounds, especially high-density lipoproteins, lysophospholipids and sphingolipids, on the expression and activity of potassium channels in human T lymphocytes is discussed.
Publication Types:
English Abstract
Research Support, Non-U.S. Gov't
Review
PMID: 10941272 [PubMed - indexed for MEDLINE]
--------------------------------------------------------------------------------
8: Q Rev Biophys. 1998 Nov;31(4):357-98.
A superfamily of small potassium channel subunits: form and function of the MinK-related peptides (MiRPs).
Abbott GW, Goldstein SA.
Department of Pediatrics, Boyer Center for Molecular Medicine, Yale University School of Medicine, New Haven, CT 06536, USA.
Publication Types:
Research Support, Non-U.S. Gov't
Research Support, U.S. Gov't, P.H.S.
Review
PMID: 10709243 [PubMed - indexed for MEDLINE]
--------------------------------------------------------------------------------
9: Curr Opin Neurobiol. 1993 Jun;3(3):283-90.
Recent advances in the understanding of potassium channel function.
Hoshi T, Zagotta WN.
University of Iowa, Iowa City.
Publication Types:
Review
PMID: 8369623 [PubMed - indexed for MEDLINE]
--------------------------------------------------------------------------------
10: Ned Tijdschr Geneeskd. 1993 May 29;137(22):1086-90.
[The ATP-sensitive potassium channel: function and potential for pharmacological modification]
[Article in Dutch]
Wilde AA.
Academisch Medisch Centrum, afd. Experimentele en Klinische Cardiologie, Amsterdam.
Publication Types:
Review
PMID: 8510783 [PubMed - indexed for MEDLINE]
--------------------------------------------------------------------------------
11: Farmakol Toksikol. 1989 May-Jun;52(3):88-93.
[Possibilities of the pharmacologic regulation of potassium channel function]
[Article in Russian]
Kasparov SA.
Potassium channels of excitable membranes are a heterogeneous group of channels among which one can distinguish potential-dependent, Ca2+-dependent, receptor-dependent and others. The substances contributing to the activation of these channels decrease excitability of membranes and the substances suppressing the activity of potassium channels increase it. A number of agents (narcotic analgetics, ligands of sigma-opiate receptors, GABA -mimetics, M-cholinergic agent) might modulate the activity of potassium channels indirectly through the corresponding receptors. Also, some drugs used in medical practice exert the immediate effect on these channels. Among them there are myotropic hypotensive drugs diazoxide, pinacidyl, BRL 34915 and minoxydyl, antidiabetic agents -- the derivatives of sulfon urea (butamide). The transfer of potassium ions through membranes is probably one of the fundamental mechanisms of the action of pharmacological agents.
Publication Types:
English Abstract
Review
PMID: 2676590 [PubMed - indexed for MEDLINE]
--------------------------------------------------------------------------------
12: Pflugers Arch. 1989;414 Suppl 1:S106-10.
Potassium channel blockers and neuronal function.
Harvey AL, Rowan EG, Anderson AJ.
Department of Physiology and Pharmacology, University of Strathclyde, Great Britain.
Publication Types:
Research Support, Non-U.S. Gov't
Review
PMID: 2674890 [PubMed - indexed for MEDLINE]
The cardiac hERG/IKr potassium channel as pharmacological target: structure, function, regulation, and clinical applications.
Thomas D, Karle CA, Kiehn J.
Department of Cardiology, Medical University Hospital Heidelberg, Im Neuenheimer Feld 410, D-69120 Heidelberg, Germany.
Human ether-a-go-go-related gene (hERG) potassium channels conduct the rapid component of the delayed rectifier potassium current, IKr, which is crucial for repolarization of cardiac action potentials. Moderate hERG blockade may produce a beneficial class III antiarrhythmic effect. In contrast, a reduction in hERG currents due to either genetic defects or adverse drug effects can lead to hereditary or acquired long QT syndromes characterized by action potential prolongation, lengthening of the QT interval on the surface ECG, and an increased risk for "torsade de pointes" arrhythmias and sudden death. This undesirable side effect of non-antiarrhythmic compounds has prompted the withdrawal of several blockbuster drugs from the market. Studies on mechanisms of hERG channel inhibition provide significant insights into the molecular factors that determine state-, voltage-, and use-dependency of hERG current block. In addition, crucial properties of the high-affinity drug binding site in hERG and its interaction with drug molecules have been identified, providing the basis for more refined approaches in drug design, safety pharmacology and in silico modeling. Recently, mutations in hERG have been shown to cause current increase and hereditary short QT syndrome with a high risk for life-threatening arrhythmias. Finally, the discovery of adrenergic mechanisms of hERG channel regulation as well as the development of strategies to enhance hERG currents and to modify intracellular hERG protein processing may provide novel antiarrhythmic options in repolarization disorders. In conclusion, the increasing understanding of hERG channel function and molecular mechanisms of hERG current regulation could improve prevention and treatment of hERG-associated cardiac repolarization disorders.
Publication Types:
Research Support, Non-U.S. Gov't
Review
PMID: 16787254 [PubMed - indexed for MEDLINE]
--------------------------------------------------------------------------------
2: Physiology (Bethesda). 2005 Dec;20:408-16.
The KCNQ1 potassium channel: from gene to physiological function.
Jespersen T, Grunnet M, Olesen SP.
Department of Medical Physiology, University of Copenhagen, Denmark.
The voltage-gated KCNQ1 (KvLQT1, Kv7.1) potassium channel plays a crucial role in shaping the cardiac action potential as well as in controlling the water and salt homeostasis in several epithelial tissues. KCNQ1 channels in these tissues are tightly regulated by auxiliary proteins and accessory factors, capable of modulating the properties of the channel complexes. This paper reviews the current knowledge about the KCNQ1 channel with a major focus on interacting proteins and physiological functions.
Publication Types:
Research Support, Non-U.S. Gov't
Review
PMID: 16287990 [PubMed - indexed for MEDLINE]
--------------------------------------------------------------------------------
3: Biochim Biophys Acta. 2003 Sep 30;1606(1-3):1-21.
Mitochondrial potassium transport: the role of the mitochondrial ATP-sensitive K(+) channel in cardiac function and cardioprotection.
Garlid KD, Dos Santos P, Xie ZJ, Costa AD, Paucek P.
Department of Biology, Portland State University, 1719 SW 10th Avenue, PO Box 751, Portland, OR 97207, USA. garlid@pdx.edu
Coronary artery disease and its sequelae-ischemia, myocardial infarction, and heart failure-are leading causes of morbidity and mortality in man. Considerable effort has been devoted toward improving functional recovery and reducing the extent of infarction after ischemic episodes. As a step in this direction, it was found that the heart was significantly protected against ischemia-reperfusion injury if it was first preconditioned by brief ischemia or by administering a potassium channel opener. Both of these preconditioning strategies were found to require opening of a K(ATP) channel, and in 1997 we showed that this pivotal role was mediated by the mitochondrial ATP-sensitive K(+) channel (mitoK(ATP)). This paper will review the evidence showing that opening mitoK(ATP) is cardioprotective against ischemia-reperfusion injury and, moreover, that mitoK(ATP) plays this role during all three phases of the natural history of ischemia-reperfusion injury preconditioning, ischemia, and reperfusion. We discuss two distinct mechanisms by which mitoK(ATP) opening protects the heart-increased mitochondrial production of reactive oxygen species (ROS) during the preconditioning phase and regulation of intermembrane space (IMS) volume during the ischemic and reperfusion phases. It is likely that cardioprotection by ischemic preconditioning (IPC) and K(ATP) channel openers (KCOs) arises from utilization of normal physiological processes. Accordingly, we summarize the results of new studies that focus on the role of mitoK(ATP) in normal cardiomyocyte physiology. Here, we observe the same two mechanisms at work. In low-energy states, mitoK(ATP) opening triggers increased mitochondrial ROS production, thereby amplifying a cell signaling pathway leading to gene transcription and cell growth. In high-energy states, mitoK(ATP) opening prevents the matrix contraction that would otherwise occur during high rates of electron transport. MitoK(ATP)-mediated volume regulation, in turn, prevents disruption of the structure-function of the IMS and facilitates efficient energy transfers between mitochondria and myofibrillar ATPases.
Publication Types:
Research Support, Non-U.S. Gov't
Research Support, U.S. Gov't, P.H.S.
Review
PMID: 14507424 [PubMed - indexed for MEDLINE]
--------------------------------------------------------------------------------
4: Am J Physiol Lung Cell Mol Physiol. 2003 May;284(5):L689-700.
Chloride and potassium channel function in alveolar epithelial cells.
O'Grady SM, Lee SY.
Department of Physiology, University of Minnesota, St. Paul, Minnesota 55108, USA. ograd001@umn.edu
Electrolyte transport across the adult alveolar epithelium plays an important role in maintaining a thin fluid layer along the apical surface of the alveolus that facilitates gas exchange across the epithelium. Most of the work published on the transport properties of alveolar epithelial cells has focused on the mechanisms and regulation of Na(+) transport and, in particular, the role of amiloride-sensitive Na(+) channels in the apical membrane and the Na(+)-K(+)-ATPase located in the basolateral membrane. Less is known about the identity and role of Cl(-) and K(+) channels in alveolar epithelial cells, but studies are revealing important functions for these channels in regulation of alveolar fluid volume and ionic composition. The purpose of this review is to examine previous work published on Cl(-) and K(+) channels in alveolar epithelial cells and to discuss the conclusions and speculations regarding their role in alveolar cell transport function.
Publication Types:
Review
PMID: 12676759 [PubMed - indexed for MEDLINE]
--------------------------------------------------------------------------------
5: Clin Exp Pharmacol Physiol. 2002 Apr;29(4):305-11.
Oxidative stress and potassium channel function.
Liu Y, Gutterman DD.
Cardiovascular Center, Medical College of Wisconsin, Milwaukee, Wisconsin 53226, USA. ypliu@mcw.edu
1. Modulation of K+ channel activities by cellular oxidative stress has emerged as a significant determinant of vasomotor function in multiple disease states. 2. Evidence from in vitro and in vivo studies suggest that superoxide (O2-) and hydrogen peroxide (H2O2) enhance BKCa channel activity in rat and cat cerebral arterioles; however, activity is decreased by peroxynitrite (ONOO-) in rat cerebral arteries. The mechanisms of changes in BKCa channel properties are not fully understood and may involve oxidation of cysteine residues that are located in the cell membranes. 3. Studies further suggest that O2- increases KATP channel activity in guinea-pig cardiac myocytes, but decreases opening in cerebral vasculature. Both H2O2 and ONOO- enhance KATP channel activity in the myocardium and in coronary, renal, mesenteric and cerebral vascular beds. Alteration of KATP channels by free radicals may be due to oxidation of SH groups or changes in the cytosolic concentration of ATP. 4. It does appear that O2- produced by either reaction of xanthine and xanthine oxidase or elevated levels of glucose reduces Kv channel activity and the impairments can be partially restored by free radical scavengers, superoxide dismutase and catalase. 5. Thus, redox modulation of potassium channel activity is an important mechanism regulating cell vascular smooth muscle membrane potential.
Publication Types:
Review
PMID: 11985541 [PubMed - indexed for MEDLINE]
--------------------------------------------------------------------------------
6: Arterioscler Thromb Vasc Biol. 2001 Jan;21(1):28-38.
Potassium channel function in vascular disease.
Sobey CG.
Department of Pharmacology, The University of Melbourne, Parkville, Victoria, Australia. cg.sobey@unimelb.edu.au
Potassium ion (K(+)) channel activity is a major regulator of vascular muscle cell membrane potential (E(m)) and is therefore an important determinant of vascular tone. There is growing evidence that the function of several types of vascular K(+) channels is altered during major cardiovascular diseases, such as chronic hypertension, diabetes, and atherosclerosis. Vasoconstriction and the compromised ability of an artery to dilate are likely consequences of defective K(+) channel function in blood vessels during these disease states. In some instances, increased K(+) channel function may help to compensate for increased vascular tone. Endothelial cell dysfunction is commonly associated with cardiovascular disease, and altered activity of nitric oxide, prostacyclin, and endothelium-derived hyperpolarizing factor could also contribute to changes in resting K(+) channel activity, E(m), and K(+) channel-mediated vasodilatation. Our current knowledge of the effects of disease on vascular K(+) channel function almost exclusively relies on interpretation of data obtained by using pharmacological modulators of K(+) channels. As further progress is made in the development of more selective drugs and through molecular approaches such as gene targeting technology in mice, specific K(+) channel abnormalities and their causes in particular diseases should be more readily identified, providing novel directions for vascular therapy.
Publication Types:
Research Support, Non-U.S. Gov't
Review
PMID: 11145930 [PubMed - indexed for MEDLINE]
--------------------------------------------------------------------------------
7: Postepy Hig Med Dosw. 2000;54(3):381-90.
[Regulation of potassium channel function in T lymphocytes by intracellular second messengers for calcium, cyclic AMP and membrane lipid metabolites]
[Article in Polish]
Teisseyre A.
Katedra i Zakład Biofizyki Akademii Medycznej we Wrocławiu.
This review focuses on the influence of well-known intracellular second messengers on the activity of potassium channels expressed in human T lymphocytes. Basic biophysical properties of the channels are briefly presented. Available data on the regulatory role of intracellular calcium and cyclic AMP is reviewed. Finally, a possible influence of lipid compounds, especially high-density lipoproteins, lysophospholipids and sphingolipids, on the expression and activity of potassium channels in human T lymphocytes is discussed.
Publication Types:
English Abstract
Research Support, Non-U.S. Gov't
Review
PMID: 10941272 [PubMed - indexed for MEDLINE]
--------------------------------------------------------------------------------
8: Q Rev Biophys. 1998 Nov;31(4):357-98.
A superfamily of small potassium channel subunits: form and function of the MinK-related peptides (MiRPs).
Abbott GW, Goldstein SA.
Department of Pediatrics, Boyer Center for Molecular Medicine, Yale University School of Medicine, New Haven, CT 06536, USA.
Publication Types:
Research Support, Non-U.S. Gov't
Research Support, U.S. Gov't, P.H.S.
Review
PMID: 10709243 [PubMed - indexed for MEDLINE]
--------------------------------------------------------------------------------
9: Curr Opin Neurobiol. 1993 Jun;3(3):283-90.
Recent advances in the understanding of potassium channel function.
Hoshi T, Zagotta WN.
University of Iowa, Iowa City.
Publication Types:
Review
PMID: 8369623 [PubMed - indexed for MEDLINE]
--------------------------------------------------------------------------------
10: Ned Tijdschr Geneeskd. 1993 May 29;137(22):1086-90.
[The ATP-sensitive potassium channel: function and potential for pharmacological modification]
[Article in Dutch]
Wilde AA.
Academisch Medisch Centrum, afd. Experimentele en Klinische Cardiologie, Amsterdam.
Publication Types:
Review
PMID: 8510783 [PubMed - indexed for MEDLINE]
--------------------------------------------------------------------------------
11: Farmakol Toksikol. 1989 May-Jun;52(3):88-93.
[Possibilities of the pharmacologic regulation of potassium channel function]
[Article in Russian]
Kasparov SA.
Potassium channels of excitable membranes are a heterogeneous group of channels among which one can distinguish potential-dependent, Ca2+-dependent, receptor-dependent and others. The substances contributing to the activation of these channels decrease excitability of membranes and the substances suppressing the activity of potassium channels increase it. A number of agents (narcotic analgetics, ligands of sigma-opiate receptors, GABA -mimetics, M-cholinergic agent) might modulate the activity of potassium channels indirectly through the corresponding receptors. Also, some drugs used in medical practice exert the immediate effect on these channels. Among them there are myotropic hypotensive drugs diazoxide, pinacidyl, BRL 34915 and minoxydyl, antidiabetic agents -- the derivatives of sulfon urea (butamide). The transfer of potassium ions through membranes is probably one of the fundamental mechanisms of the action of pharmacological agents.
Publication Types:
English Abstract
Review
PMID: 2676590 [PubMed - indexed for MEDLINE]
--------------------------------------------------------------------------------
12: Pflugers Arch. 1989;414 Suppl 1:S106-10.
Potassium channel blockers and neuronal function.
Harvey AL, Rowan EG, Anderson AJ.
Department of Physiology and Pharmacology, University of Strathclyde, Great Britain.
Publication Types:
Research Support, Non-U.S. Gov't
Review
PMID: 2674890 [PubMed - indexed for MEDLINE]
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