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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
2-5
|
pubmed:dateCreated |
1990-12-28
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pubmed:abstractText |
Although nitric oxide appears to be the major endothelium-derived relaxing factor (EDRF), it cannot explain all endothelium-dependent responses of isolated arteries. Thus, acetylcholine causes an endothelium-dependent, transient hyperpolarization, which is due to the release from the endothelial cells of a diffusible substance (endothelium-derived hyperpolarizing factor, EDHF) other than nitric oxide. The muscarinic receptors on the endothelium that trigger the release of EDHF belong to the M1-muscarinic subtype, while those activating the liberation of EDRF are M2-muscarinic in nature. The importance of endothelium-dependent hyperpolarization varies among different blood vessels. The hyperpolarization, and the resulting relaxation caused by EDHF can be attributed to an increase in K+ conductance in the vascular smooth muscle. Although the nature of EDHF remains elusive, it may be a labile metabolic of arachidonic acid.
|
pubmed:language |
eng
|
pubmed:journal | |
pubmed:citationSubset |
IM
|
pubmed:chemical | |
pubmed:status |
MEDLINE
|
pubmed:issn |
0303-6847
|
pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
27
|
pubmed:owner |
NLM
|
pubmed:authorsComplete |
Y
|
pubmed:pagination |
238-45
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pubmed:dateRevised |
2005-11-16
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pubmed:meshHeading | |
pubmed:year |
1990
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pubmed:articleTitle |
Endothelium-derived hyperpolarizing factor.
|
pubmed:affiliation |
Department of Physiology and Biophysics, Mayo Clinic, Rochester, Minn.
|
pubmed:publicationType |
Journal Article,
Review
|