Benidipine persistently inhibits delayed rectifier K+-channel currents in murine thymocytes

Itsuro Kazama, Yoshio Maruyama, Mitsunobu Matsubara

Research output: Contribution to journalArticlepeer-review

24 Citations (Scopus)


Lymphocytes predominantly express delayed rectifier K+-channels (Kv1.3) in their plasma membranes, and the channels play crucial roles in the lymphocyte activation and proliferation. Since 1,4-dihydropyridine (DHP) Ca 2+ channel blockers (CCBs), which are highly lipophilic, exert relatively stronger immunomodulatory effects than the other types of CCBs, they would affect the Kv1.3-channel currents in lymphocytes. In the present study, employing the standard patch-clamp whole-cell recording technique in murine thymocytes, we examined the effects of benidipine, one of the most lipophilic DHPs, on the channel currents and the membrane capacitance and compared them with those of nifedipine. Both drugs significantly suppressed the peak and the pulse-end currents of the channels with significant decreases in the membrane capacitance. However, the effects of benidipine were more marked than those of nifedipine and were irreversible after the drug withdrawal. This study demonstrated for the first time that DHP CCBs, such as nifedipine and benidipine, exert inhibitory effects on thymocyte Kv1.3-channel currents. The persistent effect of benidipine was thought to be associated with its sustained accumulation in the plasma membranes as detected by the long-lasting decrease in the membrane capacitance.

Original languageEnglish
Pages (from-to)28-33
Number of pages6
JournalImmunopharmacology and Immunotoxicology
Issue number1
Publication statusPublished - 2013 Feb


  • Benidipine
  • Ca channel blockers (CCBs)
  • Immunosuppressive effects
  • Kv1.3-channel
  • Lipophilicity
  • Lymphocytes
  • Membrane capacitance

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology
  • Toxicology
  • Pharmacology


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