Linked Life Data

18156169

Source:http://linkedlifedata.com/resource/pubmed/id/18156169

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
5
pubmed:dateCreated
2008-5-1
pubmed:abstractText
Mas is the receptor for angiotensin-(1-7) and is involved in cardiovascular and neuronal regulation, in which the heptapeptide also plays a major role. Mas-deficient mice have been generated by us, and their characterization has shown that Mas has important functions in behaviour and cardiovascular regulation. These mice exhibit increased anxiety but, despite an enhanced long-term potentiation in the hippocampus, do not perform better in learning experiments. When Mas-deficient mice are backcrossed to the FVB/N genetic background, a cardiovascular phenotype is uncovered, in that the backcrossed animals become hypertensive. Concordant with our detection by fluorescent in situ hybridization of Mas mRNA in mouse endothelium, this phenotype is caused by endothelial dysfunction based on a dysbalance between nitric oxide and reactive oxygen species in the vessel wall. In agreement with these data, transgenic spontaneously hypertensive stroke-prone rats overexpressing ACE2 in the vessel wall exhibit reduced blood pressure as a result of improved endothelial function. Moreover, angiotensin-(1-7) overexpression in transgenic rats has cardioprotective and haemodynamic effects. In conclusion, the angiotensin-(1-7)-Mas axis has important functional implications for vascular regulation and blood pressure control, particularly in pathophysiological situations.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
May
pubmed:issn
0958-0670
pubmed:author
pubmed:issnType
Print
pubmed:volume
93
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
528-37
pubmed:meshHeading
pubmed:year
2008
pubmed:articleTitle
Genetically altered animal models for Mas and angiotensin-(1-7).
pubmed:affiliation
Max-Delbrück-Center for Molecular Medicine (MDC), Robert-Rössle-Strasse 10, D-13092 Berlin-Buch, Germany.
pubmed:publicationType
Journal Article, Review