Mapping genes controlling hematocrit in the spontaneously hypertensive rat
Jazyk angličtina Země Spojené státy americké Médium print
Typ dokumentu časopisecké články, práce podpořená grantem, Research Support, U.S. Gov't, P.H.S.
Grantová podpora
P01 HL-35018
NHLBI NIH HHS - United States
PubMed
9166579
DOI
10.1007/s003359900452
Knihovny.cz E-zdroje
- MeSH
- chromozomy MeSH
- erythropoetin genetika MeSH
- genetická vazba MeSH
- genetické markery MeSH
- hematokrit * MeSH
- inbrední kmeny potkanů MeSH
- krevní tlak fyziologie MeSH
- krysa rodu Rattus MeSH
- lidé MeSH
- mapování chromozomů metody MeSH
- myši MeSH
- potkani inbrední SHR genetika MeSH
- rekombinace genetická MeSH
- zvířata MeSH
- Check Tag
- krysa rodu Rattus MeSH
- lidé MeSH
- myši MeSH
- zvířata MeSH
- Publikační typ
- časopisecké články MeSH
- práce podpořená grantem MeSH
- Research Support, U.S. Gov't, P.H.S. MeSH
- Názvy látek
- erythropoetin MeSH
- genetické markery MeSH
The genes that determine the baseline hematocrit level in humans and experimental animals are unknown. The spontaneously hypertensive rat (SHR), the most widely used animal model of human essential hypertension, exhibits an increased hematocrit when compared with the normotensive Brown Norway (BN-Lx) strain (0.54 +/- 0.02 vs. 0.44 +/- 0.02, p < 0.01). Distribution of hematocrit values among recombinant inbred (RI) strains derived from SHR and BN-Lx progenitors was continuous, which suggests a polygenic mode of inheritance. The narrow heritability of the hematocrit was estimated to be 0.32. The Eno2 marker on Chromosome (Chr) 4 showed the strongest association (p < 0.0001) with the observed variability of hematocrit among RI strains. The erythropoietin (Epo) gene, originally reported to be syntenic with Eno2, has been mapped to Chr 12, thus excluding it as a potential candidate gene for the increased hematocrit in the SHR. The current linkage data extend homologies between rat, mouse, and human chromosomes.
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