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| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
2 Pt 2
|
| pubmed:dateCreated |
1987-5-18
|
| pubmed:abstractText |
Present evidence indicates that the active metabolite SIN-1 of the prodrug molsidomine dilates vascular smooth muscle and inhibits platelet aggregation by a direct stimulatory effect on soluble guanylate-cyclase in the cytosol of vascular smooth muscle cells and platelets, respectively. Evidence from studies in bovine coronary arteries is presented to proof the causal relation between SIN-1 induced rises in cGMP and relaxation under a variety of pharmacological conditions. In contrast to organic nitrates, SIN-1, which activates guanylate-cyclase in vitro independently of the presence of added cysteine, does not cause tolerance. Tolerance most pronounced with nitroglycerin appears to be due to a direct inactivating effect of this drug on guanylate-cyclase.
|
| pubmed:language |
fre
|
| pubmed:journal | |
| pubmed:citationSubset |
IM
|
| pubmed:chemical | |
| pubmed:status |
MEDLINE
|
| pubmed:month |
Feb
|
| pubmed:issn |
0369-8114
|
| pubmed:author | |
| pubmed:issnType |
Print
|
| pubmed:volume |
35
|
| pubmed:owner |
NLM
|
| pubmed:authorsComplete |
Y
|
| pubmed:pagination |
260-5
|
| pubmed:dateRevised |
2006-11-15
|
| pubmed:meshHeading | |
| pubmed:year |
1987
|
| pubmed:articleTitle |
[Mechanism of the vasodilating effect and blood platelet- antiaggregating activity of molsidomine and SIN-1].
|
| pubmed:publicationType |
Journal Article,
English Abstract
|