RGD Reference Report - Contribution of autosomal loci and the Y chromosome to the stress response in rats. - Rat Genome Database

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Contribution of autosomal loci and the Y chromosome to the stress response in rats.

Authors: Dumas, P  Pausova, Z  Kren, V  Krenova, D  Pravenec, M  Dumont, M  Ely, D  Turner, M  Sun, Y  Tremblay, J  Hamet, P 
Citation: Dumas P, etal., Hypertension 2000 Feb;35(2):568-73
RGD ID: 61094
Web Url: http://hyper.ahajournals.org/cgi/content/abstract/35/2/568
Pubmed: PMID:10679499   (View Abstract at PubMed)

Stress is a critical contributor to cardiovascular diseases through its impact on blood pressure variability and cardiac function. Familial clustering of reactivity to stress has been demonstrated in human subjects, and some rodent models of hypertension are hyperresponsive to stress. Therefore, the present study was designed to uncover the genetic determinants of the stress response. We performed a total genome linkage search to identify the loci of the body temperature response to immobilization stress in a set of recombinant inbred strains (RIS) originating from reciprocal crosses of spontaneously hypertensive rats (SHR) with a normotensive Brown Norway Lx strain. Two quantitative trait loci (QTLs) were revealed on chromosomes (Chrs) 10 and 12 (logarithm of odds scores, 2.2 and 1. 3, respectively). The effects of these QTLs were enhanced by a high sodium diet (logarithm of odds scores, 4.0 and 3.3 for Chrs 10 and 12, respectively), which is suggestive of a salt-sensitive component for the phenotype. Congenics for Chr 10 confirmed both the QTL and the salt effect in RIS. Negatively associated loci were also identified on Chrs 8 and 11. Interaction between the loci of Chrs 10 and 12 was demonstrated, with the rat strains bearing SHR alleles at both loci having the highest thermal response to stress. Furthermore, the Y Chr of SHR origin enhanced the response to immobilization stress, as demonstrated in 2 independent models, RIS and Y Chr consomics. However, its full effect requires autosomes of the SHR strain. These findings provide the first evidence for the genetic determination of reactivity to stress with interactions between autosomal loci and between the Y and autosomal Chrs that contribute to the explanation of the 46% of variance in the stress response.



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Mammalian Phenotype

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Strains with Phenominer Data Strains with phenominer data
SHR/Ola SHR-Chr YWKY/Akr WKY-Chr YSHR/Akr
SHR-Chr YBN/Cub WKY/OlaHsd

Objects Annotated

QTLs
Btemp1  (Thermal response to stress QTL 1)
Btemp2  (Thermal response to stress QTL 2)

Strains
BN-Lx/Cub  (Brown Norway with polydactyly-luxate)
SHR-Chr YBN/Cub  (NA)
SHR-Chr YWKY/Akr  (NA)
SHR.BN-(D10Mit4-D10Wox11)/Cub  (NA)
SHR/NHsd  (NA)
SHR/Ola  (NA)

Objects referenced in this article
Gene Myh3 myosin heavy chain 3 Rattus norvegicus
Strain WKY-Chr YSHR/Akr null Rattus norvegicus

Additional Information