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PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
1999-2-17
pubmed:abstractText
a fpreviously produced angiotensinogen-deficient mice, i.e. mice with deleted renin-angiotensin system (RAS), with a genetic background on C57BL/6J - C57BL/6J-agt (-/-) -, but no C57BL/6J-agt (-/-) which survived long enough to be weaned. In the present study, we attempted to prevent neonatal death and analyzed pathological development in C57BL/6J-agt (-/-). We indicate that mortality in C57BL/6J-agt (-/-) derived from C57BL/6J-agt (+/-) can be reduced by hypodermic saline injection in the 7 days following birth, that hydronephrosis developed by day 14 in association with polydiplasia and polyuria by day 30, and that chronic hypotension occurs. Hydronephrosis is less damaging to electrolyte resorption in younger mice, but not in adults. We also observed that C57BL/6J-agt (-/-) derived from C57BL/6J-agt (-/-) frequently develop fetal hydronephrosis and die of respiratory failure at birth. These results suggest that maternal RAS is associated with structural maturation of kidney and lung in late fetus and that postnatal RAS plays important roles in structural and functional maintenance of the kidneys.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Mar
pubmed:issn
1107-3756
pubmed:author
pubmed:issnType
Print
pubmed:volume
1
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
583-7
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
1998
pubmed:articleTitle
Pathologic characterization of hypotensive C57BL/6J-agt: angiotensinogen-deficient C57BL/6J mice.
pubmed:affiliation
Laboratory Animal Research Center, University of Tsukuba, Ibaraki 305, Japan.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't