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| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
1
|
| pubmed:dateCreated |
1997-3-25
|
| pubmed:abstractText |
1. In primary hypertension, an abnormally high vascular resistance can be explained in terms of alterations in vessel wall structure. Arterial cell hypertrophy and/or hyperplasia have been implicated as playing a central role in the vascular abnormalities noted in spontaneously hypertensive rats (SHR). Cultured arterial cells appear therefore as attractive models for studying in vitro the mechanisms whereby cells originating from hypertensives exhibit hyperproliferation and/or hyperresponsiveness. 2. This review summarized our present knowledge on growth and related biochemical events of cultured SHR-derived vascular smooth muscle cells or aortic adventitial fibroblasts, in response to various polypeptide growth factors and vasoactive agents. 3. Exaggerated growth response to various mitogens in cultured SHR-derived vascular cells has been well documented. However, the molecular mechanisms of abnormal growth in SHR remain unknown. This abnormality seems not to be a consequence of the alterations at the levels of receptors or of some key mitogenic events of early signalling pathways such as phospholipase C, protein kinase C and G-proteins. Further studies should therefore focus on the more distal events related to cell growth.
|
| pubmed:language |
eng
|
| pubmed:journal | |
| pubmed:citationSubset |
IM
|
| pubmed:status |
MEDLINE
|
| pubmed:month |
Dec
|
| pubmed:issn |
0143-9294
|
| pubmed:author | |
| pubmed:issnType |
Print
|
| pubmed:volume |
22
|
| pubmed:owner |
NLM
|
| pubmed:authorsComplete |
Y
|
| pubmed:pagination |
S114-6
|
| pubmed:dateRevised |
2006-11-15
|
| pubmed:meshHeading | |
| pubmed:year |
1995
|
| pubmed:articleTitle |
Molecular mechanisms of vascular hypertrophy in the spontaneously hypertensive rat.
|
| pubmed:affiliation |
Groupe de Signalisation, Universite Rene Descartes, Paris, France.
|
| pubmed:publicationType |
Journal Article,
Review,
Research Support, Non-U.S. Gov't
|