RGD Reference Report - Genetic Loci contribute to the progression of vascular and cardiac hypertrophy in salt-sensitive spontaneous hypertension. - Rat Genome Database

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Genetic Loci contribute to the progression of vascular and cardiac hypertrophy in salt-sensitive spontaneous hypertension.

Authors: Siegel, AK  Planert, M  Rademacher, S  Mehr, AP  Kossmehl, P  Wehland, M  Stoll, M  Kreutz, R 
Citation: Siegel AK, etal., Arterioscler Thromb Vasc Biol 2003 Jul 1;23(7):1211-7.
RGD ID: 629621
Pubmed: PMID:12775577   (View Abstract at PubMed)
DOI: DOI:10.1161/01.ATV.0000079509.20542.C9   (Journal Full-text)

OBJECTIVE: The salt-sensitive Dahl rat and the spontaneously hypertensive rat develop comparable spontaneous hypertension on a low-salt diet, whereas only the salt-sensitive Dahl rat strain develops a striking increase in blood pressure and cardiovascular hypertrophy on a high-salt diet. We set out to identify quantitative trait loci (QTLs) contributing to the progression of salt-induced organ damage in hypertension by studying an F2 population derived from both strains. METHODS AND RESULTS: We determined systolic blood pressure (SBP), vascular aortic hypertrophy (AH), cardiac left ventricular (LV) hypertrophy (LVH), and LV fibrosis in 230 male F2-animals on a high-salt diet. A strong correlation between AH and LVH was found (r=0.58, P<0.0001), and genome-wide QTL mapping detected suggestive or significant QTLs in overlapping chromosomal fragments for AH and LVH on chromosomes 1, 3, and 19, respectively. A significant influence of SBP on the extent of LVH and AH was evident at all QTLs, although significant linkage to SBP (together with LVH) was only found on chromosome 9. No QTLs for LV fibrosis were detected. CONCLUSIONS: This study demonstrates a strong correlation between AH and LVH in salt-sensitive hypertension and identifies QTLs contributing to the progression of cardiovascular hypertrophy in this condition.

RGD Manual Disease Annotations    Click to see Annotation Detail View
TermQualifierEvidenceWithReferenceNotesSourceOriginal Reference(s)
Cardiac Fibrosis  IAGP 629621on 4% NaCl dietRGD 
heart disease  IDA 629621; 629621; 629621 RGD 
hypertension  IDA 629621; 629621; 629621; 629621; 629621; 629621; 629621 RGD 
Left Ventricular Hypertrophy  IDA 629621; 629621; 629621 RGD 

Phenotype Annotations    Click to see Annotation Detail View

Mammalian Phenotype

TermQualifierEvidenceWithReferenceNotesSourceOriginal Reference(s)
abnormal aortic weight  QTM 629621; 629621; 629621 RGD 
cardiac interstitial fibrosis  IAGP 629621on 4% NaCl dietRGD 
heart left ventricle hypertrophy  QTM 629621; 629621; 629621 RGD 
increased aortic weight  IAGP 629621compared to SHR/FubRkb on 4% NaCl dietRGD 
increased heart left ventricle weight  IAGP 629621compared to SHR/FubRkb on 4% NaCl dietRGD 
increased systemic arterial blood pressure  QTM 629621 RGD 
increased systemic arterial blood pressure  IAGP 629621compared to SHR/FubRkb on 4% NaCl dietRGD 
Objects Annotated

QTLs
Bp108  (Blood pressure QTL 108)
Cm10  (Cardiac mass QTL 10)
Cm11  (Cardiac mass QTL 11)
Cm12  (Cardiac mass QTL 12)
Cm7  (Cardiac mass QTL 7)
Cm8  (Cardiac mass QTL 8)
Cm9  (Cardiac mass QTL 9)

Strains
SHR/FubRkb  (NA)
SS/JrRkb  (NA)


Additional Information