The role of potassium channels in the vasodilatory effect of levosimendan in human internal thoracic arteries

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Usta C., eksert B., Golbasi I., Bigat Z., Ozdem S. S.

EUROPEAN JOURNAL OF CARDIO-THORACIC SURGERY, cilt.30, sa.2, ss.329-332, 2006 (SCI-Expanded) identifier identifier identifier

  • Yayın Türü: Makale / Tam Makale
  • Cilt numarası: 30 Sayı: 2
  • Basım Tarihi: 2006
  • Doi Numarası: 10.1016/j.ejcts.2006.05.019
  • Dergi Adı: EUROPEAN JOURNAL OF CARDIO-THORACIC SURGERY
  • Derginin Tarandığı İndeksler: Science Citation Index Expanded (SCI-EXPANDED), Scopus
  • Sayfa Sayıları: ss.329-332
  • Anahtar Kelimeler: levosimendan, potassium channel, human internal thoracic artery, vasodilatation, SENSITIVE K+ CHANNEL, CARDIAC TROPONIN-C, CALCIUM SENSITIZER, CA2+ SENSITIZER, HEART, INODILATOR, PIG
  • Akdeniz Üniversitesi Adresli: Evet

Özet

Objective: We investigated the role of potassium channels in vasodilatory effect of levosimendan in human internal thoracic arteries. Methods: Samples of redundant internal thoracic arteries obtained from patients undergoing a coronary artery bypass graft surgery were cut into 3 mm wide rings and suspended in 20 ml organ baths. Isometric tension was continuously measured with an isometric force transducer connected to a computer-based data acquisition system. Results: Levosimendan (10(-8) -10(-5) M) or cromakalim (10(-8) -10(-5) M) produced concentration-dependent relaxation responses in human internal thoracic arteries precontracted by 10(-6) M phenylephrine. The relaxant responses to levosimendan did not differ significantly between endothelium-intact and endothelium-denuded preparations. Incubation of human internal thoracic artery rings with adenosine 3',5'-triphosphate (ATP)-dependent potassium channel blocker glibenclamide (10(-6) M) for 30 min significantly inhibited the relaxant responses to both levosimendan and cromakatim. The Ca2+-activated potassium channel blocker iberiotoxin (10(-7) M) also caused a significant but smaller inhibition on relaxant responses to levosimendan. Incubation of the rings with the voltage-dependent potassium channel. blocker 4-aminopyridine (5 mM) for 10 min did not cause significant alterations in relaxant responses to levosimendan. Conclusions: The findings of this study suggested that levosimendan-induced relaxation responses in human internal thoracic arteries were depended on the activation of ATP-dependent and Ca2+-activated potassium channels. (c) 2006 Elsevier B.V. All rights reserved.

Objective: We investigated the role of potassium channels in vasodilatory effect of levosimendan in human internal thoracic arteries. Methods: Samples of redundant internal thoracic arteries obtained from patients undergoing a coronary artery bypass graft surgery were cut into 3 mm wide rings and suspended in 20 ml organ baths. Isometric tension was continuously measured with an isometric force transducer connected to a computer-based data acquisition system. Results: Levosimendan (10(-8) -10(-5) M) or cromakalim (10(-8) -10(-5) M) produced concentration-dependent relaxation responses in human internal thoracic arteries precontracted by 10(-6) M phenylephrine. The relaxant responses to levosimendan did not differ significantly between endothelium-intact and endothelium-denuded preparations. Incubation of human internal thoracic artery rings with adenosine 3',5'-triphosphate (ATP)-dependent potassium channel blocker glibenclamide (10(-6) M) for 30 min significantly inhibited the relaxant responses to both levosimendan and cromakatim. The Ca2+-activated potassium channel blocker iberiotoxin (10(-7) M) also caused a significant but smaller inhibition on relaxant responses to levosimendan. Incubation of the rings with the voltage-dependent potassium channel. blocker 4-aminopyridine (5 mM) for 10 min did not cause significant alterations in relaxant responses to levosimendan. Conclusions: The findings of this study suggested that levosimendan-induced relaxation responses in human internal thoracic arteries were depended on the activation of ATP-dependent and Ca2+-activated potassium channels. (c) 2006 Elsevier B.V. All rights reserved.