Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
6
pubmed:dateCreated
1994-4-21
pubmed:abstractText
The description of pathogenetic mechanisms underlying different genetic models of essential hypertension is a useful way of illustrating the logical sequence needed to dissect a complex phenotypic condition such as hypertension. The abnormalities in renal function observed in spontaneously hypertensive rats of the Okamoto strain and Milan strain will be emphasized. The description may proceed "downward" from alterations that affect the whole body function to cellular and subcellular levels. However, the identification in the Milan strain rats of a point mutation in the gene coding for adducin, a skeletal protein able to modulate transepithelial sodium transport, provides the opportunity to reconstruct, in an "upward" direction, the sequence of events leading from the single point mutation to the final complex phenotype of essential hypertension.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:status
MEDLINE
pubmed:month
Dec
pubmed:issn
0931-041X
pubmed:author
pubmed:issnType
Print
pubmed:volume
7
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
865-70
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
1993
pubmed:articleTitle
Genetic models of arterial hypertension--role of tubular ion transport.
pubmed:affiliation
Division of Nephrology, Dialysis and Hypertension, University of Milan, Italy.
pubmed:publicationType
Journal Article, Review, Research Support, Non-U.S. Gov't