| PKC inhibitors prevent endothelial dysfunction after myocardial ischemia-reperfusion in rats. | |
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MedLine Citation:
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PMID: 8928868 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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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. |
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Authors:
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K Numaguchi; H Shimokawa; R Nakaike; K Egashira; A Takeshita |
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Publication Detail:
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Type: Journal Article; Research Support, Non-U.S. Gov't |
Journal Detail:
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Title: The American journal of physiology Volume: 270 ISSN: 0002-9513 ISO Abbreviation: Am. J. Physiol. Publication Date: 1996 May |
Date Detail:
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Created Date: 1996-11-27 Completed Date: 1996-11-27 Revised Date: 2007-11-15 |
Medline Journal Info:
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Nlm Unique ID: 0370511 Medline TA: Am J Physiol Country: UNITED STATES |
Other Details:
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Languages: eng Pagination: H1634-9 Citation Subset: IM |
Affiliation:
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Research Institute of Angiocardiology, Kyushu University School of Medicine, Fukuoka Japan. |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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Animals Endothelium, Vascular / drug effects*, physiopathology Enzyme Activation Male Myocardial Ischemia / physiopathology* Myocardial Reperfusion* Peptides, Cyclic / pharmacology Protein Kinase C / antagonists & inhibitors* Rats Rats, Inbred WKY Receptors, Endothelin / antagonists & inhibitors Reperfusion Injury / physiopathology Tetradecanoylphorbol Acetate / pharmacology Vasodilation / drug effects, physiology |
| Chemical | |
Reg. No./Substance:
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0/Peptides, Cyclic; 0/Receptors, Endothelin; 136553-81-6/cyclo(Trp-Asp-Pro-Val-Leu); 16561-29-8/Tetradecanoylphorbol Acetate; EC 2.7.11.13/Protein Kinase C |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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