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Naunyn-Schmiedeberg's Archives of Pharmacology

, Volume 356, Issue 6, pp 853–855 | Cite as

Cardioprotective effect against ischemia-reperfusion injury of AHC-52, a dihydropyridine compound with inhibitory effect on Cl– but not Ca2+ current

  • H. Tanaka
  • Toshiyuki Sekine
  • Miyuki Terada
  • Yoshiro Kobayashi
  • Koki Shigenobu
Short communication

Abstract

We examined the effects of a dihydropyridine compound, AHC-52, on guinea pig myocardium. In ventricular cardiomyocytes, AHC-52 (1 μM) had no effect on the basal peak inward and steady state currents, but inhibited the isoprenaline-induced time independent Cl current. In coronary perfused right ventricular preparations, no-flow ischemia induced decreases in developed tension which recovered only to about 50% of initial values after reperfusion. AHC-52 (0.1 μM) had no effect on developed tension under normal conditions and during ischemia, but significantly improved the recovery of developed tension after reperfusion to about 80% of preischemic values. Thus, AHC-52 inhibits Cl channels in cardiac muscle and may have protective effects against ischemia-reperfusion injury.

Key words Cardioprotection AHC-52 Chloride current Dihydropyridine Ischemia-reperfusion 

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Copyright information

© Springer-Verlag Berlin Heidelberg 1997

Authors and Affiliations

  • H. Tanaka
    • 1
  • Toshiyuki Sekine
    • 1
  • Miyuki Terada
    • 1
  • Yoshiro Kobayashi
    • 2
  • Koki Shigenobu
    • 1
  1. 1.Department of Pharmacology, Toho University School of Pharmaceutical Sciences, Miyama 2-2-1 Funabashi, Chiba 274, JapanJP
  2. 2.Faculty of Science, Toho University, Miyama 2-2-1 Funabashi, Chiba 274, JapanJP

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