Linked Life Data

9973259

Source:http://linkedlifedata.com/resource/pubmed/id/9973259

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
1999-5-3
pubmed:abstractText
Targeted disruption of mineralocorticoid receptor (MR) gene results in pseudohypoaldosteronism type I with failure to thrive, severe dehydration, hyperkalemia, hyponatremia, and high plasma levels of renin, angiotensin II, and aldosterone. In this study, mRNA expression of the different components of the renin-angiotensin system (RAS) were evaluated in liver, lung, heart, kidney and adrenal gland to assess their response to a state of extreme sodium depletion. Angiotensinogen, renin, angiotensin-I converting enzyme, and angiotensin II receptor (AT1 and AT2) mRNA expressions were determined by Northern blot and RT-PCR analysis. Furthermore, in situ hybridization and immunohistochemistry allowed us to identify the cell types involved in the variation of the RAS component expression. In the heterozygous mice (MR+/-), compared with wild-type mice (MR+/+), there was no significant variation of any mRNA of the RAS components. In MR knockout mice (MR-/-), compared with wild-type mice, there were significant increases in the expression level of several RAS components. In the liver, angiotensinogen and AT1 receptor mRNA expressions were moderately stimulated. In the kidney, renin mRNA was increased up to 10-fold and in situ hybridization showed a marked recruitment of renin-producing cells; however, the levels of angiotensin-I converting enzyme mRNA and AT1 mRNA were not changed. Interestingly, in adrenal gland, renin expression was also strongly up-regulated in a thickened zona glomerulosa, whereas AT1 mRNA expression remained unchanged. Altogether, these results demonstrate that in the MR knockout mice model, RAS component expressions are differentially altered, renin being the most stimulated component. Angiotensinogen and AT1 in the liver are also increased, but the other elements of the RAS are not affected.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Feb
pubmed:issn
0888-8809
pubmed:author
pubmed:issnType
Print
pubmed:volume
13
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
297-306
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed-meshheading:9973259-Adrenal Glands, pubmed-meshheading:9973259-Angiotensin II, pubmed-meshheading:9973259-Angiotensinogen, pubmed-meshheading:9973259-Animals, pubmed-meshheading:9973259-Blotting, Northern, pubmed-meshheading:9973259-Female, pubmed-meshheading:9973259-Gene Expression Regulation, pubmed-meshheading:9973259-Heart, pubmed-meshheading:9973259-Immunohistochemistry, pubmed-meshheading:9973259-In Situ Hybridization, pubmed-meshheading:9973259-Kidney, pubmed-meshheading:9973259-Liver, pubmed-meshheading:9973259-Lung, pubmed-meshheading:9973259-Male, pubmed-meshheading:9973259-Mice, pubmed-meshheading:9973259-Mice, Inbred C57BL, pubmed-meshheading:9973259-Mice, Knockout, pubmed-meshheading:9973259-Peptidyl-Dipeptidase A, pubmed-meshheading:9973259-RNA, pubmed-meshheading:9973259-Receptors, Mineralocorticoid, pubmed-meshheading:9973259-Renin, pubmed-meshheading:9973259-Renin-Angiotensin System, pubmed-meshheading:9973259-Reverse Transcriptase Polymerase Chain Reaction, pubmed-meshheading:9973259-Sodium
pubmed:year
1999
pubmed:articleTitle
Effects of mineralocorticoid receptor gene disruption on the components of the renin-angiotensin system in 8-day-old mice.
pubmed:affiliation
INSERM U36-Laboratoire de Médecine Expérimentale, Collège de France, Paris. chubert@infobiogen.fr
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't