Resveratrol-induced depression of the mechanical and electrical activities of the rat heart is reversed by glyburide: Evidence for possible KATP channels activation


Buluc M., Ayaz M., TURAN B., DEMİREL YILMAZ E.

Archives of Pharmacal Research, vol.30, no.5, pp.603-607, 2007 (SCI-Expanded) identifier identifier identifier

  • Publication Type: Article / Article
  • Volume: 30 Issue: 5
  • Publication Date: 2007
  • Doi Number: 10.1007/bf02977655
  • Journal Name: Archives of Pharmacal Research
  • Journal Indexes: Science Citation Index Expanded (SCI-EXPANDED), Scopus
  • Page Numbers: pp.603-607
  • Keywords: resveratrol, rat heart, contraction, membrane potential, K-ATP channels, ISCHEMIA-REPERFUSION INJURY, SENSITIVE POTASSIUM CHANNEL, NITRIC-OXIDE, RED WINE, VENTRICULAR MYOCYTES, TRANS-RESVERATROL, ACTION-POTENTIALS, SMOOTH-MUSCLE, GUINEA-PIGS, INCREASE
  • Lokman Hekim University Affiliated: No

Abstract

Resveratrol, a natural phytoalexin found in wine, has been suggested to have benefits in preventing cardiovascular diseases. However, the direct effects of resveratrol on the activity of cardiac tissues and its mechanism of action have not been determined. This study examined the effects of resveratrol on the right and left atrium and left papillary muscle isolated from the rat heart. The contractile responses of the right atrium and papillary muscle and the action potential from the left atrium were recorded and the effects of resveratrol on these responses were observed. The resting force of the isolated right atrium and the peak developed force of the left papillary muscle were depressed by resveratrol (0.1 nM - 0.1 mM). Exposure to the KATP channel blocker glyburide (3 μM) prevented significantly the resveratrol-induced decrease. Resveratrol (0.1 mM) shortened the repolarization phase of action potential recorded from the left atrium and this effect of resveratrol was reversed by glyburide (3 μM). These results indicated that resveratrol depressed cardiac muscle contraction and shortened action potential duration probably due to the activation of KATP channels in the rat heart.