ArticleBritish journal of pharmacology2003
Dihydropyridine Ca2+ channel antagonists and agonists block Kv4.2, Kv4.3 and Kv1.4 K+ channels expressed in HEK293 cells.
Article in British journal of pharmacology, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 38 citations in OpenAlex.
- Acute arsenic trioxide inhibits the cardiac transient outward KCurrent research in structural biology · 2026Article
- Voltage-gated ion channels mediate the electrotaxis of glioblastoma cells in a hybrid PMMA/PDMS microdevice.APL bioengineering · 2020Article
- Discovery and Development of Calcium Channel Blockers.Frontiers in pharmacology · 2017Review
- Effects of neferine on Kv4.3 channels expressed in HEK293 cells and ex vivo electrophysiology of rabbit hearts.Acta pharmacologica Sinica · 2015Article
- Effect of tyrphostin AG879 on Kv 4.2 and Kv 4.3 potassium channels.British journal of pharmacology · 2015Article
- Effect of the I(to) activator NS5806 on cloned K(V)4 channels depends on the accessory protein KChIP2.British journal of pharmacology · 2010Article
- Dihydropyridine block of voltage-dependent K+ currents in rat dorsal root ganglion neurons.Neuroscience · 2009Article
- The transmembrane beta-subunits KCNE1, KCNE2, and DPP6 modify pharmacological effects of the antiarrhythmic agent tedisamil on the transient outward current Ito.Naunyn-Schmiedeberg's archives of pharmacology · 2009Article
- Modification of K+ channel-drug interactions by ancillary subunits.The Journal of physiology · 2008Review
- Mechanisms of endothelin-1-induced decrease in contractility in adult mouse ventricular myocytes.British journal of pharmacology · 2007Article
- Molecular mechanisms of regulation of fast-inactivating voltage-dependent transient outward K+ current in mouse heart by cell volume changes.The Journal of physiology · 2005Article
- Effects of diltiazem and nifedipine on transient outward and ultra-rapid delayed rectifier potassium currents in human atrial myocytes.British journal of pharmacology · 2005Article
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Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
(1) We have determined the molecular basis of nicardipine-induced block of cardiac transient outward K(+) currents (I(to)). Inhibition of I(to) was studied using cloned voltage-dependent K(+) channels (Kv) channels, rat Kv4.3L, Kv4.2, and Kv1.4, expressed in human embryonic kidney cell line 293 (HEK293) cells. (2) Application of the dihydropyridine Ca(2+) channel antagonist, nicardipine, accelerated the inactivation rate and reduced the peak amplitude of Kv4.3L currents in a concentration-dependent manner (IC(50): 0.42 micro M). The dihydropyridine (DHP) Ca(2+) channel agonist, Bay K 8644, also blocked this K(+) current (IC(50): 1.74 micro M). (3) Nicardipine (1 micro M) slightly, but significantly, shifted the voltage dependence of activation and steady-state inactivation to more negative potentials, and also slowed markedly the recovery from inactivation of Kv4.3L currents. (4) Coexpression of K(+) channel-interacting protein 2 (KChIP2) significantly slowed the inactivation of Kv4.3L currents as expected. However, the features of DHP-induced block of K(+) current were not substantially altered. (5) Nicardipine exhibited similar block of Kv1.4 and Kv4.2 channels stably expressed in HEK293 cells; IC(50)'s were 0.80 and 0.62 micro M, respectively. (6) Thus, at submicromolar concentrations, DHP Ca(2+) antagonist and agonist inhibit Kv4.3L and have similar inhibiting effects on other components of cardiac I(to), Kv4.2 and Kv1.4.
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