ArticleThe Journal of clinical investigation1996
Quantitative trait loci influencing cholesterol and phospholipid phenotypes map to chromosomes that contain genes regulating blood pressure in the spontaneously hypertensive rat.
Article in The Journal of clinical investigation, 1996. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 87 citations in OpenAlex.
- Research on Experimental Hypertension in Prague (1966-2009).Physiological research · 2024Article
- Nutrigenetic Interaction of Spontaneously Hypertensive Rat Chromosome 20 Segment and High-Sucrose Diet Sensitizes to Metabolic Syndrome.Nutrients · 2022Article
- Complement Factor B Is a Determinant of Both Metabolic and Cardiovascular Features of Metabolic Syndrome.Hypertension (Dallas, Tex. : 1979) · 2017Article
- Serum Triglyceride Lowering Effect of Cilnidipine in Patients With Essential Hypertension.Cardiology research · 2016Article
- Atherogenic Risk Assessment among Persons Living in Rural Uganda.Journal of tropical medicine · 2016Article
- Chromosomal assignment of quantitative trait loci influencing baseline circulating total cholesterol level in male laboratory mice: report of a consomic strain survey and comparison with published results.BMC research notes · 2015Article
- Genomic determinants of triglyceride and cholesterol distribution into lipoprotein fractions in the rat.PloS one · 2014Article
- LIPITENSION: Interplay between dyslipidemia and hypertension.Indian journal of endocrinology and metabolism · 2012Article
- Integrated genomic approaches to identification of candidate genes underlying metabolic and cardiovascular phenotypes in the spontaneously hypertensive rat.Physiological genomics · 2011Article
- Refined mapping of the renal failure RF-3 quantitative trait locus.Journal of the American Society of Nephrology : JASN · 2011Article
- Genetic control of plasma lipid levels in a cross derived from normoglycaemic Brown Norway and spontaneously diabetic Goto-Kakizaki rats.Diabetologia · 2006Article
- Statins: another class of antihypertensive agents?Journal of human hypertension · 2006Review
- Use of a dense single nucleotide polymorphism map for in silico mapping in the mouse.PLoS biology · 2004Article
- Article
- Genetics of Cd36 and the clustering of multiple cardiovascular risk factors in spontaneous hypertension.The Journal of clinical investigation · 1999Article
- Mapping genes controlling hematocrit in the spontaneously hypertensive rat.Mammalian genome : official journal of the International Mammalian Genome Society · 1997Article
Corrections and comments
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Authors and funding
13 authors at 5 institutions in 3 countries.
Funding
Abstract
The frequent coincidence of hypertension and dyslipidemia suggests that related genetic factors might underlie these common risk factors for cardiovascular disease. To investigate whether quantitative trait loci (QTLs) regulating lipid levels map to chromosomes known to contain genes regulating blood pressure, we used a genome scanning approach to map QTLs influencing cholesterol and phospholipid phenotypes in a large set of recombinant inbred strains and in congenic strains derived from the spontaneously hypertensive rat and normotensive Brown-Norway (BN.Lx) rat fed normal and high cholesterol diets. QTLs regulating lipid phenotypes were mapped by scanning the genome with 534 genetic markers. A significant relationship (P < 0.00006) was found between basal HDL2 cholesterol levels and the D19Mit2 marker on chromosome 19. Analysis of congenic strains of spontaneously hypertensive rat indicated that QTLs regulating postdietary lipid phenotypes exist also on chromosomes 8 and 20. Previous studies in the recombinant inbred and congenic strains have demonstrated the presence of blood pressure regulatory genes in corresponding segments of chromosomes 8, 19, and 20. These findings provide support for the hypothesis that blood pressure and certain lipid subfractions can be modulated by linked genes or perhaps even the same genes.
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