Molecular basis for the lack of HERG K+ channel block-related cardiotoxicity by the H1 receptor blocker cetirizine compared with other second-generation antihistamines

Mol Pharmacol. 1998 Jul;54(1):113-21. doi: 10.1124/mol.54.1.113.

Abstract

In the current study, the potential blocking ability of K+ channels encoded by the human ether-a-go-go related gene (HERG) by the piperazine H1 receptor antagonist cetirizine has been examined and compared with that of other second-generation antihistamines (astemizole, terfenadine, and loratadine). Cetirizine was completely devoid of any inhibitory action on HERG K+ channels heterologously expressed in Xenopus laevis oocytes in concentrations up to 30 microM. On the other hand, terfenadine and astemizole effectively blocked HERG K+ channels with nanomolar affinities (the estimated IC50 values were 330 and 480 nM, respectively), whereas loratadine was approximately 300-fold less potent (IC50 approximately 100 microM). In addition, in contrast to terfenadine, cetirizine did not show use-dependent blockade. In SH-SY5Y cells, a human neuroblastoma clone that constitutively expresses K+ currents carried by HERG channels (IHERG), as well as in human embryonic kidney 293 cells stably transfected with HERG cDNA, extracellular perfusion with 3 microM cetirizine did not exert any inhibitory action on IHERG. Astemizole (3 microM), on the other hand, was highly effective. Terfenadine (3 microM) caused a marked (approximately 80%) inhibition of IHERG in SH-SY5Y cells, whereas loratadine, at the same concentration, caused a 40% blockade. Furthermore, the application of cetirizine (3 microM) on the intracellular side of the membrane of HERG-transfected human embryonic kidney 293 cells did not affect IHERG, whereas the same intracellular concentration of astemizole caused a complete block. The results of the current study suggest that second-generation antihistamines display marked differences in their ability to block HERG K+ channels. Cetirizine in particular, which possesses more polar and smaller substituent groups attached to the tertiary amine compared with other antihistamines, lacks HERG-blocking properties, possibly explaining the absence of torsade de pointes ventricular arrhythmias associated with its therapeutical use.

Publication types

  • Comparative Study
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Astemizole / pharmacology
  • Cation Transport Proteins*
  • Cetirizine / pharmacology*
  • DNA-Binding Proteins*
  • ERG1 Potassium Channel
  • Electrophysiology
  • Ether-A-Go-Go Potassium Channels
  • Female
  • Heart / drug effects*
  • Heart / physiology
  • Histamine H1 Antagonists / pharmacology*
  • Humans
  • Loratadine / pharmacology
  • Oocytes / drug effects
  • Oocytes / metabolism
  • Potassium Channels / drug effects*
  • Potassium Channels / metabolism
  • Potassium Channels, Voltage-Gated*
  • Receptors, Histamine H1 / drug effects*
  • Receptors, Histamine H1 / metabolism
  • Terfenadine / pharmacology
  • Trans-Activators*
  • Transcriptional Regulator ERG
  • Transfection
  • Tumor Cells, Cultured / drug effects
  • Xenopus laevis

Substances

  • Cation Transport Proteins
  • DNA-Binding Proteins
  • ERG protein, human
  • ERG1 Potassium Channel
  • Ether-A-Go-Go Potassium Channels
  • Histamine H1 Antagonists
  • KCNH2 protein, human
  • KCNH6 protein, human
  • Potassium Channels
  • Potassium Channels, Voltage-Gated
  • Receptors, Histamine H1
  • Trans-Activators
  • Transcriptional Regulator ERG
  • Loratadine
  • Terfenadine
  • Astemizole
  • Cetirizine

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