ArticleThe Journal of clinical investigation1998
Construction of a double congenic strain to prove an epistatic interaction on blood pressure between rat chromosomes 2 and 10.
Article in The Journal of clinical investigation, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed.
- Modularity/non-cumulativity of quantitative trait loci on blood pressure.Journal of human hypertension · 2020Review
- Genetic predisposition for increased red blood cell distribution width is an early risk factor for cardiovascular and renal comorbidities.Disease models & mechanisms · 2020Article
- Towards Precision Medicine for Hypertension: A Review of Genomic, Epigenomic, and Microbiomic Effects on Blood Pressure in Experimental Rat Models and Humans.Physiological reviews · 2017Review
- Widespread epistasis regulates glucose homeostasis and gene expression.PLoS genetics · 2017Article
- Dr Lewis Kitchener Dahl, the Dahl rats, and the "inconvenient truth" about the genetics of hypertension.Hypertension (Dallas, Tex. : 1979) · 2015Article
- Do epistatic modules exist in the genetic control of blood pressure in Dahl rats? A critical perspective.Physiological genomics · 2013Article
- Isolation and high-throughput sequencing of two closely linked epistatic hypertension susceptibility loci with a panel of bicongenic strains.Physiological genomics · 2013Article
- FOXO1 orchestrates the bone-suppressing function of gut-derived serotonin.The Journal of clinical investigation · 2012Article
- The kidney and hypertension: pathogenesis of salt-sensitive hypertension.Current hypertension reports · 2012Review
- Use of contiguous congenic strains in analyzing compound QTLs.Physiological genomics · 2012Article
- Rac1 GTPase in rodent kidneys is essential for salt-sensitive hypertension via a mineralocorticoid receptor-dependent pathway.The Journal of clinical investigation · 2011Article
- Epistatic genetic determinants of blood pressure and mortality in a salt-sensitive hypertension model.Hypertension (Dallas, Tex. : 1979) · 2009Article
- Investigating the effect of genetic background on proteinuria and renal injury using two hypertensive strains.American journal of physiology. Renal physiology · 2009Article
- Contrasting epistatic interactions between rat quantitative trait loci controlling mammary cancer development.Mammalian genome : official journal of the International Mammalian Genome Society · 2009Article
- Closely linked non-additive blood pressure quantitative trait loci.Mammalian genome : official journal of the International Mammalian Genome Society · 2008Article
- Quantitative trait loci associated with blood pressure of metabolic syndrome in the progeny of NZO/HILtJxC3H/HeJ intercrosses.Mammalian genome : official journal of the International Mammalian Genome Society · 2007Article
- Epistasis between hyperglycemic QTLs revealed in a double congenic of the OLETF rat.Mammalian genome : official journal of the International Mammalian Genome Society · 2007Article
- Functional genomics in rodent models of hypertension.The Journal of physiology · 2004Review
- Article
- Strategy for uncovering complex determinants of hypertension using animal models.Current hypertension reports · 2000Review
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3 authors.
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Abstract
Previously we presented suggestive evidence from an F2 segregating population for an interaction on blood pressure (BP) between quantitative trait loci (QTL) on rat chromosomes (Chr) 2 and 10. To prove the existence of such an interaction, we developed congenic strains for Chr 2 and 10 by introgressing the low BP QTL alleles into the Dahl salt-sensitive (S) strain. A double congenic strain was also constructed with both the Chr 2 and 10 low BP QTL alleles on the S background. The four strains (S, Chr 2 congenic, Chr 10 congenic, and Chr 2/10 double congenic) were studied for BP response to increased salt intake. An analysis of variance showed significant main effects of Chr 2, Chr 10, and a significant interaction between Chr 2 and 10 on BP and heart weight (all P < 0.0001). The interaction accounted for 24 mmHg of BP and 79 mg of heart weight. Thus, the discovery and proof of epistatic interactions are clearly critical to understanding the genetics of blood pressure.
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