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HSP27 locus cosegregates with left ventricular mass independently of blood pressure.

https://arctichealth.org/en/permalink/ahliterature54596
Source
Hypertension. 1996 Dec;28(6):1112-7
Publication Type
Article
Date
Dec-1996
Author
P. Hamet
M A Kaiser
Y. Sun
V. Pagé
M. Vincent
V. Kren
M. Pravenec
J. Kunes
J. Tremblay
N J Samani
Author Affiliation
Centre de Recherche Hôtel-Dieu de Montréal, Université de Montréal, Canada.
Source
Hypertension. 1996 Dec;28(6):1112-7
Date
Dec-1996
Language
English
Publication Type
Article
Keywords
Alleles
Animals
Autoradiography
Blood Pressure - genetics
Heat-Shock Proteins - genetics
Hypertrophy, Left Ventricular - genetics
Male
Polymerase Chain Reaction
Rats
Rats, Inbred SHR
Rats, Inbred WKY
Research Support, Non-U.S. Gov't
Abstract
Left ventricular hypertrophy remains a significant clinical problem and a predictor of fatal outcome in hypertension. Blood pressure per se and environmental modifiers including stress affect cardiac mass. Heat shock proteins are involved in the stress response as well as in the regulation of cardiac growth and cytoprotection. The present study evaluates heat shock protein 27 as a locus marker or candidate gene of cardiac hypertrophy in hypertension. The spontaneously hypertensive rat allele of heat shock protein 27 was associated with about a 6% increase in relative left ventricular weight (P = .0112) in 30 recombinant inbred strains from crosses of Brown Norway and spontaneously hypertensive rats. In 336 F2 crosses of spontaneously hypertensive and Wistar-Kyoto rats, the hypertensive allele was dominant and cosegregated with a similar 6% increase in the ratio of left ventricular weight to body weight (P = .0058) in rats fed a normal salt diet, but its contribution to left ventricular weight decreased in rats kept on a high salt diet. The contribution of the heat shock protein 27 allele was independent of blood pressure. We suggest that heat shock protein 27 represents a candidate gene/locus marker of cardiac hypertrophy in hypertension.
PubMed ID
8952607 View in PubMed
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Mapping of genetic determinants of the sympathoneural response to stress.

https://arctichealth.org/en/permalink/ahliterature76094
Source
Physiol Genomics. 2005 Jan 20;20(2):183-7
Publication Type
Article
Date
Jan-20-2005
Author
I. Klimes
K. Weston
D. Gasperíková
P. Kovács
R. Kvetnanský
D. Jezová
R. Dixon
J R Thompson
E. Seböková
N J Samani
Author Affiliation
Diabetes and Nutrition Research Laboratory, Slovak Academy of Sciences, Bratislava, Slovakia.
Source
Physiol Genomics. 2005 Jan 20;20(2):183-7
Date
Jan-20-2005
Language
English
Publication Type
Article
Keywords
Animals
Blood pressure
Catecholamines - metabolism
Chromosome Mapping
Computational Biology
Crosses, Genetic
Epinephrine - blood
Female
Genetic markers
Genotype
Linkage (Genetics)
Lod Score
Male
Microsatellite Repeats
Norepinephrine - blood
Phenotype
Quantitative Trait Loci
Rats
Rats, Inbred BN
Research Support, Non-U.S. Gov't
Species Specificity
Stress
Sympathetic Nervous System - pathology
Time Factors
Variation (Genetics)
Abstract
Activation of the sympathoadrenal system (SAS, comprising the sympathetic nervous system and the adrenal medulla) in response to stressful stimuli is an important defense mechanism as well as a contributor to several cardiovascular diseases. There is variability in the SAS response to stress, although the extent to which this is genetically regulated is unclear. Some rodent models, including the hereditary hypertriglyceridemic (hHTg) rat, are hyperresponsive to stress. We investigated whether quantitative trait loci (QTLs) that affect sympathoadrenal response to stress could be identified. Second filial generation rats (n = 189) derived from a cross of the hHTg rat and the Brown Norway rat had plasma norepinephrine (NE) and epinephrine (Epi) levels, indices of activation of the sympathoneural and adrenal medulla components, respectively, measured in the resting state and in response to an immobilization stress. Responses were assessed early (20 min) and late (120 min) after the application of the stress. A genome scan was conducted using 153 microsatellite markers. Two QTLs (maximum peak LOD scores of 4.17 and 3.52, respectively) influencing both the early and late plasma NE response to stress were found on chromosome 10. Together, the QTLs accounted for approximately 20% of the total variation in both the early and late NE responses in the F(2) rats. Interestingly, the QTLs had no effect on plasma Epi response to stress. These findings provide evidence for a genetic determination of the response of a specific component of the SAS response to stress. Genetically determined variation in sympathetic nervous system response to stress may contribute to cardiovascular diseases.
PubMed ID
15547139 View in PubMed
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Mapping of genetic loci predisposing to hypertriglyceridaemia in the hereditary hypertriglyceridaemic rat: analysis of genetic association with related traits of the insulin resistance syndrome.

https://arctichealth.org/en/permalink/ahliterature53563
Source
Diabetologia. 2003 Mar;46(3):352-8
Publication Type
Article
Date
Mar-2003
Author
I. Klimes
K. Weston
P. Kovacs
D. Gasperikova
D. Jezova
R. Kvetnansky
J R Thompson
E. Sebokova
N J Samani
Author Affiliation
Diabetes and Nutrition Research Laboratory, Institute of Experimental Endocrinology, Slovak Academy of Sciences, Bratislava, Slovakia.
Source
Diabetologia. 2003 Mar;46(3):352-8
Date
Mar-2003
Language
English
Publication Type
Article
Keywords
Animals
Blood Glucose - genetics - metabolism
Blood Pressure - genetics
Chromosome Mapping
Chromosomes - genetics
DNA - genetics - isolation & purification
Female
Genetic markers
Hypertriglyceridemia - genetics
Insulin - blood - genetics
Insulin Resistance - genetics
Male
Phenotype
Rats
Rats, Inbred BN
Research Support, Non-U.S. Gov't
Abstract
AIMS/HYPOTHESIS: Hypertriglyceridaemia is an important risk factor for coronary heart disease, especially in the context of the insulin resistance syndrome where it often occurs with hypertension. The two phenotypes are also associated in the hereditary hypertriglyceridaemic (hHTg) rat. The aim of this study was to map quantitative trait loci that affect plasma triglyceride concentration in the hHTg rat and determine whether they co-localize with loci for blood pressure. METHODS: Second filial generation progeny (n=189) from a cross of the hHTg rat with the Brown Norway rat were phenotyped for fasting plasma triglyceride, glucose and insulin concentrations, and direct unrestrained resting blood pressure. A partial genome-scan was conducted using 153 microsatellite markers that were polymorphic between the two strains. RESULTS: A major locus (lod score 6.5) influencing plasma triglyceride concentration in a co-dominant fashion was mapped to chromosome 4 between D1Mit 5 and D1Mit17. Chromosome 8 contained multiple peaks with a lod score greater than 4.0 influencing triglyceride concentration. Importantly, none of the triglyceride loci had an effect on blood pressure. The triglyceride locus on chromosome 4 co-localized with a locus for fasting plasma insulin (lod score 4.1), although the effect on insulin concentration was in the opposite direction to that on triglyceride. CONCLUSION/INTERPRETATION: We have mapped the major loci that affect plasma triglyceride concentration in the hHTg rat. These loci do not influence blood pressure suggesting that these commonly associated phenotypes of the insulin resistance syndrome are not be due to pleiotropic effects of the same gene(s).
PubMed ID
12687333 View in PubMed
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