Diclofenac, a non-steroidal anti-inflammatory drug, inhibits L-type Ca 2+ channels in neonatal rat ventricular cardiomyocytes

Oleg V. Yarishkin, Eun Mi Hwang, Donggyu Kim, Jae Cheal Yoo, Sang Soo Kang, Deok Ryoung Kim, Jae Hee Jung Shin, Hye Joo Chung, Ho Sang Jeong, Dawon Kang, Jaehee Han, Jae Yong Park, Seong Geun Hong

Research output: Contribution to journalArticlepeer-review

29 Citations (Scopus)


A non-steroidal anti-inflammatory drug (NSAID) has many adverse effects including cardiovascular (CV) risk. Diclofenac among the nonselective NSAIDs has the highest CV risk such as congestive heart failure, which resulted commonly from the impaired cardiac pumping due to a disrupted excitation-contraction (E-C) coupling. We investigated the effects of diclofenac on the L-type calcium channels which are essential to the E-C coupling at the level of single ventricular myocytes isolated from neonatal rat heart, using the whole-cell voltage-clamp technique. Only diclofenac of three NSAIDs, including naproxen and ibuprofen, significantly reduced inward whole cell currents. At concentrations higher than 3 μM, diclofenac inhibited reversibly the Na+ current and did irreversibly the L-type Ca2+ channels-mediated inward current (IC50=12.89±0.43 μM) in a dose-dependent manner. However, nifedipine, a well-known L-type channel blocker, effectively inhibited the L-type Ca2+ currents but not the Na+ current. Our finding may explain that diclofenac causes the CV risk by the inhibition of L-type Ca2+ channel, leading to the impairment of E-C coupling in cardiac myocytes.

Original languageEnglish
Pages (from-to)437-442
Number of pages6
JournalKorean Journal of Physiology and Pharmacology
Issue number6
Publication statusPublished - 2009 Dec
Externally publishedYes


  • Diclofenac
  • L-type Ca current
  • Rat cardiac myocytes

ASJC Scopus subject areas

  • Physiology
  • Pharmacology


Dive into the research topics of 'Diclofenac, a non-steroidal anti-inflammatory drug, inhibits L-type Ca 2+ channels in neonatal rat ventricular cardiomyocytes'. Together they form a unique fingerprint.

Cite this