Modulation of potassium channels by antiarrhythmic and antihypertensive drugs.

Agents that modulate cardiac and smooth muscle K+ channels have stimulated considerable interest in recent years because of their therapeutic potential in a number of cardiovascular diseases. Foremost among these drugs are the so-called Class III antiarrhythmic agents, which act by prolonging cardiac action potentials, and K+ channel openers, which hyperpolarize and thereby relax smooth muscle cells. Many of the newly developed Class III antiarrhythmic agents probably act by specific block of one subtype of delayed rectifier K+ current, IKr, whereas other agents block more than one type of cardiac K+ current. Much controversy exists over the specific type of K+ channel (or channels) in smooth muscle that are activated by the K+ channel openers. Both groups of K+ channel modulators have great therapeutic promise, but the Class III antiarrhythmic agents may suffer from a side-effect that is directly linked to their specific mechanism of action.

[1]  P. Gosse,et al.  [Mechanisms of ventricular tachycardia]. , 1993, Archives des maladies du coeur et des vaisseaux.

[2]  D. Roden,et al.  Suppression of time-dependent outward current in guinea pig ventricular myocytes. Actions of quinidine and amiodarone. , 1991, Circulation research.

[3]  M. Leppert,et al.  Linkage of a cardiac arrhythmia, the long QT syndrome, and the Harvey ras-1 gene. , 1991, Science.

[4]  H. Kuriyama,et al.  Pinacidil inhibits the ryanodine‐sensitive outward current and glibenclamide antagonizes its action in cells from the rabbit portal vein , 1991, British journal of pharmacology.

[5]  N. Castle Selective inhibition of potassium currents in rat ventricle by clofilium and its tertiary homolog. , 1991, The Journal of pharmacology and experimental therapeutics.

[6]  J. Mclarnon,et al.  Actions of cardiac drugs on a calcium-dependent potassium channel in hippocampal neurons. , 1991, Molecular pharmacology.

[7]  M. Gwilt,et al.  Electrophysiologic Properties of UK‐66,914, a Novel Class III Antiarrhythmic Agent , 1991, Journal of cardiovascular pharmacology.

[8]  A. W. Jones,et al.  Stimulation of arterial 42K efflux by ATP depletion and cromakalim is antagonized by glyburide. , 1991, The American journal of physiology.

[9]  M. Sanguinetti,et al.  Delayed rectifier outward K+ current is composed of two currents in guinea pig atrial cells. , 1991, The American journal of physiology.

[10]  J. Arrowsmith,et al.  UK-68,798: a novel, potent and highly selective class III antiarrhythmic agent which blocks potassium channels in cardiac cells. , 1991, The Journal of pharmacology and experimental therapeutics.

[11]  W. Lederer,et al.  ATP-sensitive potassium channel modulation of the guinea pig ventricular action potential and contraction. , 1991, Circulation research.

[12]  M. Sanguinetti,et al.  Isoproterenol antagonizes prolongation of refractory period by the class III antiarrhythmic agent E-4031 in guinea pig myocytes. Mechanism of action. , 1991, Circulation research.

[13]  T. Colatsky,et al.  Channel specificity in antiarrhythmic drug action. Mechanism of potassium channel block and its role in suppressing and aggravating cardiac arrhythmias. , 1990, Circulation.

[14]  G. Grover,et al.  Reduction of ischemic damage in isolated rat hearts by the potassium channel opener, RP 52891. , 1990, European journal of pharmacology.

[15]  H. Hatt,et al.  Two different types of potassium channels in human skeletal muscle activated by potassium channel openers , 1990, Neuroscience Letters.

[16]  I Findlay,et al.  Action potential duration and activation of ATP-sensitive potassium current in isolated guinea-pig ventricular myocytes. , 1990, Biochimica et biophysica acta.

[17]  W. Lederer,et al.  Modulation of ATP-sensitive K+ channel activity and contractile behavior in mammalian ventricle by the potassium channel openers cromakalim and RP49356. , 1990, The Journal of pharmacology and experimental therapeutics.

[18]  Z. Fan,et al.  Multiple actions of pinacidil on adenosine triphosphate‐sensitive potassium channels in guinea‐pig ventricular myocytes. , 1990, The Journal of physiology.

[19]  F. Marumo,et al.  Interrelation between pinacidil and intracellular ATP concentrations on activation of the ATP-sensitive K+ current in guinea pig ventricular myocytes. , 1990, Circulation research.

[20]  S. Silberberg,et al.  An ATP, calcium and voltage sensitive potassium channel in porcine coronary artery smooth muscle cells. , 1990, Biochemical and biophysical research communications.

[21]  S. Silberberg,et al.  ATP inhibits smooth muscle Ca2+-activated K+ channels , 1990, Proceedings of the Royal Society of London. Series B: Biological Sciences.

[22]  G. Edwards,et al.  Structure-activity relationships of K+ channel openers. , 1990, Trends in pharmacological sciences.

[23]  D. Roden,et al.  Suppression of repolarization-related arrhythmias in vitro and in vivo by low-dose potassium channel activators. , 1990, Circulation.

[24]  M J Janse,et al.  Potassium accumulation in the globally ischemic mammalian heart. A role for the ATP-sensitive potassium channel. , 1990, Circulation research.

[25]  D. Roden,et al.  Time-dependent outward current in guinea pig ventricular myocytes. Gating kinetics of the delayed rectifier , 1990, The Journal of general physiology.

[26]  M. Oike,et al.  Nicorandil opens a calcium-dependent potassium channel in smooth muscle cells of the rat portal vein. , 1990, The Journal of pharmacology and experimental therapeutics.

[27]  H. Refsum,et al.  Rate‐Dependent Class III Antiarrhythmic Action, Negative Chronotropy, and Positive Inotropy of a Novel Ik Blocking Drug, UK‐68,798: Potent in Guinea Pig but no Effect in Rat Myocardium , 1990, Journal of cardiovascular pharmacology.

[28]  L. Carlsson,et al.  QTU‐Prolongation and Torsades de Pointes Induced by Putative Class III Antiarrhythmic Agents in the Rabbit: Etiology and Interventions , 1990, Journal of cardiovascular pharmacology.

[29]  M. Morad,et al.  Tedisamil blocks the transient and delayed rectifier K+ currents in mammalian cardiac and glial cells. , 1990, The Journal of pharmacology and experimental therapeutics.

[30]  J B Patlak,et al.  Calcium channels, potassium channels, and voltage dependence of arterial smooth muscle tone. , 1990, The American journal of physiology.

[31]  M. Sanguinetti,et al.  Two components of cardiac delayed rectifier K+ current. Differential sensitivity to block by class III antiarrhythmic agents , 1990, The Journal of general physiology.

[32]  D. Robertson,et al.  Potassium channel modulators: scientific applications and therapeutic promise. , 1990, Journal of medicinal chemistry.

[33]  M. Hiraoka,et al.  Effects of a Novel Class III Antiarrhythmic Agent, E‐4031, on Reentrant Tachycardias in Rabbit Right Atrium , 1990, Journal of cardiovascular pharmacology.

[34]  G. Grover,et al.  Nicorandil Improves postischemic Contractile function Independently of Direct Mycardial.Effects , 1990, Journal of cardiovascular pharmacology.

[35]  H. Selnick,et al.  Suppression of Lethal Ischemic Ventricular Arrhythmias by the Class III Agent E4031 in a Canine Model of Previous Myocardial Infarction , 1990, Journal of cardiovascular pharmacology.

[36]  W. Lederer,et al.  The regulation of ATP‐sensitive K+ channel activity in intact and permeabilized rat ventricular myocytes. , 1990, The Journal of physiology.

[37]  R. Stein,et al.  Cloning and expression of the delayed-rectifier IsK channel from neonatal rat heart and diethylstilbestrol-primed rat uterus. , 1990, Proceedings of the National Academy of Sciences of the United States of America.

[38]  J. Daut,et al.  Hypoxic dilation of coronary arteries is mediated by ATP-sensitive potassium channels. , 1990, Science.

[39]  M. Dunne Effects of pinacidil, RP 49356 and nicorandil on ATP‐sensitive potassium channels in insulin‐secreting cells , 1990, British journal of pharmacology.

[40]  D. Snyders,et al.  Class III antiarrhythmic agents have a lot of potential but a long way to go. Reduced effectiveness and dangers of reverse use dependence. , 1990, Circulation.

[41]  O. Petersen,et al.  The effects of cromakalim on ATP‐sensitive potassium channels in insulin‐secreting cells , 1990, British journal of pharmacology.

[42]  A. Terano,et al.  Glibenclamide specifically blocks ATP-sensitive K+ channel current in atrial myocytes of guinea pig heart. , 1990, Japanese journal of pharmacology.

[43]  F. Ashcroft,et al.  Properties and functions of ATP-sensitive K-channels. , 1990, Cellular signalling.

[44]  P. Mulder,et al.  Cardiovascular and biological effects of K+ channel openers, a class of drugs with vasorelaxant and cardioprotective properties. , 1990, Life sciences.

[45]  M. Horie,et al.  Two types of delayed rectifying K+ channels in atrial cells of guinea pig heart. , 1990, The Japanese journal of physiology.

[46]  S. Duty,et al.  Potassium channel openers. Pharmacological effects and future uses. , 1990, Drugs.

[47]  G. Edwards,et al.  Potassium channel openers and vascular smooth muscle relaxation. , 1990, Pharmacology & therapeutics.

[48]  W. Lederer,et al.  Nucleotide modulation of the activity of rat heart ATP‐sensitive K+ channels in isolated membrane patches. , 1989, The Journal of physiology.

[49]  R. Kass,et al.  Activation of ATP-sensitive K channels in heart cells by pinacidil: dependence on ATP. , 1989, The American journal of physiology.

[50]  E. Carmeliet,et al.  Delayed K+ current and external K+ in single cardiac Purkinje cells. , 1989, The American journal of physiology.

[51]  D. Escande,et al.  Apparent competition between ATP and the potassium channel opener RP 49356 on ATP-sensitive K+ channels of cardiac myocytes. , 1989, Molecular pharmacology.

[52]  H. Tanaka,et al.  Time- and voltage-dependent block of the delayed K+ current by quinidine in rabbit sinoatrial and atrioventricular nodes. , 1989, The Journal of pharmacology and experimental therapeutics.

[53]  E. Deroubaix,et al.  Effects of activation of ATP-sensitive K+ channels in mammalian ventricular myocytes. , 1989, The American journal of physiology.

[54]  T. Bolton,et al.  Properties of the cromakalim‐induced potassium conductance in smooth muscle cells isolated from the rabbit portal vein , 1989, British journal of pharmacology.

[55]  G. Grover,et al.  Anti-ischemic effects of the potassium channel activators pinacidil and cromakalim and the reversal of these effects with the potassium channel blocker glyburide. , 1989, The Journal of pharmacology and experimental therapeutics.

[56]  T. Colatsky,et al.  K+ Channel Blockers and Activators in Cardiac Arrhythmias , 1989 .

[57]  N. Lodge,et al.  A Ca2+-activated K+ channel from rabbit aorta: modulation by cromakalim. , 1989, European journal of pharmacology.

[58]  A. Coenen,et al.  K+ channel openers decrease seizures in genetically epileptic rats. , 1989, European journal of pharmacology.

[59]  M. Sanguinetti,et al.  Influence of ATP-sensitive potassium channel modulators on ischemia-induced fibrillation in isolated rat hearts. , 1989, Journal of molecular and cellular cardiology.

[60]  N. Standen,et al.  Hyperpolarizing vasodilators activate ATP-sensitive K+ channels in arterial smooth muscle. , 1989, Science.

[61]  Godfrey L. Smith,et al.  Simultaneous Measurements of Action Potential Duration and Intracellular ATP in Isolated Ferret Hearts Exposed to Cyanide , 1989, Circulation research.

[62]  R. Stein,et al.  Glyburide blocks the relaxation response to BRL 34915 (cromakalim), minoxidil sulfate and diazoxide in vascular smooth muscle. , 1989, The Journal of pharmacology and experimental therapeutics.

[63]  S. Nakanishi,et al.  Cloning of a membrane protein that induces a slow voltage-gated potassium current. , 1988, Science.

[64]  M. Sanguinetti,et al.  BRL 34915 (cromakalim) activates ATP-sensitive K+ current in cardiac muscle. , 1988, Proceedings of the National Academy of Sciences of the United States of America.

[65]  D. Escande,et al.  The potassium channel opener cromakalim (BRL 34915) activates ATP-dependent K+ channels in isolated cardiac myocytes. , 1988, Biochemical and biophysical research communications.

[66]  R. Kass,et al.  Block of heart potassium channels by clofilium and its tertiary analogs: relationship between drug structure and type of channel blocked. , 1988, Molecular pharmacology.

[67]  J. Ruskin,et al.  Electrophysiologic effects of d-sotalol in humans. , 1987, Journal of the American College of Cardiology.

[68]  T. Shibasaki,et al.  Conductance and kinetics of delayed rectifier potassium channels in nodal cells of the rabbit heart. , 1987, The Journal of physiology.

[69]  A Shrier,et al.  Repolarization currents in embryonic chick atrial heart cell aggregates. , 1986, Biophysical journal.

[70]  T. Hamilton,et al.  Comparison of the effects of BRL 34915 and verapamil on electrical and mechanical activity in rat portal vein , 1986, British journal of pharmacology.

[71]  E. Carmeliet Electrophysiologic and voltage clamp analysis of the effects of sotalol on isolated cardiac muscle and Purkinje fibers. , 1985, The Journal of pharmacology and experimental therapeutics.

[72]  B. Lucchesi,et al.  Antiarrhythmic and antifibrillatory actions of the levo- and dextrorotatory isomers of sotalol. , 1984, Journal of cardiovascular pharmacology.

[73]  A. Noma,et al.  ATP-regulated K+ channels in cardiac muscle , 1983, Nature.

[74]  D. Attwell,et al.  Membrane potential and ion concentration stability conditions for a cell with a restricted extracellular space , 1979, Proceedings of the Royal Society of London. Series B. Biological Sciences.

[75]  M. I. Steinberg,et al.  Clofilum--a new antifibrillatory agent that selectively increases cellular refractoriness. , 1979, Life sciences.

[76]  D. Noble,et al.  Outward membrane currents activated in the plateau range of potentials in cardiac Purkinje fibres , 1969, The Journal of physiology.