PKC inhibitors prevent endothelial dysfunction after myocardial ischemia-reperfusion in rats

Kohtaro Numaguchi, Hiroaki Shimokawa, Ryuichi Nakaike, Kensuke Egashira, Akira Takeshita

研究成果: ジャーナルへの寄稿記事

29 引用 (Scopus)

抜粋

The intracellular mecha-nism for endothelial dysfunction after myocardial ischemia-reperfusion remains to be elucidated. It has been reported that activation of protein kinase C (PKC) occurs after myocardial ischemia-reperfusion and that the activation impairs endothelium-dependent relaxation. Thus we examined the role of PKC activation in the ischemia-reperfusion-induced endothelial dysfunction. Isolated rat hearts perfused with a constant flow were subjected to global ischemia for 15 min followed by reperfusion for 20 min. Coronary vascular responses to the endothelium-dependent vasodilators acetylcholine (ACh) and bradykinin (BK) and the endothelium-independent vasodilator sodium nitroprusside (SNP) were examined before and after the ischemia-reperfusion. Endothelium-dependent relaxations to ACh and BK were impaired after the ischemia-reperfusion, whereas endothelium-independent relaxations to SNP were unaffected. Pretreatment with a PKC inhibitor, staurosporine, H7, or calphostin C, prevented the impairments. Phorbol 12-myristate 13-acetate, a PKC-activating phorbol ester, attenuated the relaxations to ACh and BK but not those to SNP. These results suggest that PKC activation may be involved in part in the ischemia-reperfusion-induced endothelial dysfunction.

元の言語英語
ページ(範囲)H1634-H1639
ジャーナルAmerican Journal of Physiology - Heart and Circulatory Physiology
270
発行部数5 39-5
出版物ステータス出版済み - 12 1 1996

    フィンガープリント

All Science Journal Classification (ASJC) codes

  • Physiology
  • Cardiology and Cardiovascular Medicine
  • Physiology (medical)

これを引用

Numaguchi, K., Shimokawa, H., Nakaike, R., Egashira, K., & Takeshita, A. (1996). PKC inhibitors prevent endothelial dysfunction after myocardial ischemia-reperfusion in rats. American Journal of Physiology - Heart and Circulatory Physiology, 270(5 39-5), H1634-H1639.