Document Detail

PKC inhibitors prevent endothelial dysfunction after myocardial ischemia-reperfusion in rats.
MedLine Citation:
PMID:  8928868     Owner:  NLM     Status:  MEDLINE    
The intracellular mechanism 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.
K Numaguchi; H Shimokawa; R Nakaike; K Egashira; A Takeshita
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  The American journal of physiology     Volume:  270     ISSN:  0002-9513     ISO Abbreviation:  Am. J. Physiol.     Publication Date:  1996 May 
Date Detail:
Created Date:  1996-11-27     Completed Date:  1996-11-27     Revised Date:  2007-11-15    
Medline Journal Info:
Nlm Unique ID:  0370511     Medline TA:  Am J Physiol     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  H1634-9     Citation Subset:  IM    
Research Institute of Angiocardiology, Kyushu University School of Medicine, Fukuoka Japan.
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MeSH Terms
Endothelium, Vascular / drug effects*,  physiopathology
Enzyme Activation
Myocardial Ischemia / physiopathology*
Myocardial Reperfusion*
Peptides, Cyclic / pharmacology
Protein Kinase C / antagonists & inhibitors*
Rats, Inbred WKY
Receptors, Endothelin / antagonists & inhibitors
Reperfusion Injury / physiopathology
Tetradecanoylphorbol Acetate / pharmacology
Vasodilation / drug effects,  physiology
Reg. No./Substance:
0/Peptides, Cyclic; 0/Receptors, Endothelin; 136553-81-6/cyclo(Trp-Asp-Pro-Val-Leu); 16561-29-8/Tetradecanoylphorbol Acetate; EC Kinase C

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