Mapping genes controlling hematocrit in the spontaneously hypertensive rat |
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| Authors: | M. Pravenec V. Zidek M. Zdobinska V. Kren D. Krenova A. Bottger L. F. M. van Zutphen J. -M. Wang E. St. Lezin |
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| Affiliation: | (1) Institute of Physiology, Academy of Sciences of the Czech Republic, Vídenská 1083, 142 20 Prague 4, Czech Republic, CS;(2) Institute of Biology, 1st Medical Faculty, Charles University, 128 00 Prague 2, Czech Republic, CS;(3) Department of Laboratory Animal Science, Faculty of Veterinary Medicine, Utrecht University, Utrecht, Netherlands, NL;(4) Department of Laboratory Medicine, University of California, San Francisco, California 94143-0134, USA, US |
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| Abstract: | 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. Received: 11 December 1996 / Accepted: 17 February 1997 |
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