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Nacitarhan C, Bayram Z, Eksert B, Usta C, Golbasi I, Ozdem SS: The effect of hydrogen peroxide in human internal thoracic arteries: role of potassium channels, nitric oxide and cyclooxygenase products. Cardiovasc Drugs Ther. 2007 Aug;21(4):257-62.
INTRODUCTION: We investigated both the effect and the role (s) of potassium channels, nitric oxide (NO) and cyclooxygenase (COX) products in the effect of hydrogen peroxide (H (2) O (2)) in human internal thoracic artery (ITA) rings. MATERIALS AND METHODS: Samples of redundant ITA 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: H (2) O (2) (10 (-7)-10 (-4) M) produced concentration-dependent relaxation responses in human ITA precontracted by phenylephrine. The relaxant responses to H (2) O (2) did not differ significantly between endothelium-intact and endothelium-denuded preparations. Incubation of human ITA rings with superoxide dismutase (50 U/ml) did not affect the relaxant responses to H (2) O (2), while 1,000 U/ml catalase caused a significant decrease. Incubation of endothelium-intact or endothelium-denuded human ITA rings with voltage-dependent potassium channel blocker 4-aminopyridine (5 mM) significantly inhibited the relaxant responses to H (2) O (2). COX inhibitor indomethacin (10 (-5) M) also caused a significant inhibition. Incubation with ATP-dependent potassium channel blocker glibenclamide (10 (-6) M) or Ca (2+)-activated potassium channel blocker iberiotoxin (10 (-7) M) or NO synthase (NOS) blocker N (omega)-nitro-L: -arginine methyl ester (10 (-4) M) did not alter relaxant responses of ITA rings to H (2) O (2). CONCLUSION: The findings of the present study suggested that H (2) O (2)-induced relaxation responses in human ITA were neither dependant on the endothelium nor blocked by NOS inhibition but they rather seem to depend on the activation of voltage-dependent potassium channels and COX. |
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