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

Send us a Message



Submit Data |  Help |  Video Tutorials |  News |  Publications |  Download |  REST API |  Citing RGD |  Contact   

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

  
Object SymbolSpeciesTermQualifierEvidenceWithNotesSourceOriginal Reference(s)
SS/JrRkbRatCardiac Fibrosis  IAGP on 4% NaCl dietRGD 
Cm7Ratheart disease  IDA  RGD 
Cm8Ratheart disease  IDA  RGD 
Cm9Ratheart disease  IDA  RGD 
Bp108Rathypertension  IDA  RGD 
Cm10Rathypertension  IDA  RGD 
Cm11Rathypertension  IDA  RGD 
Cm12Rathypertension  IDA  RGD 
Cm7Rathypertension  IDA  RGD 
Cm8Rathypertension  IDA  RGD 
Cm9Rathypertension  IDA  RGD 
Cm10RatLeft Ventricular Hypertrophy  IDA  RGD 
Cm11RatLeft Ventricular Hypertrophy  IDA  RGD 
Cm12RatLeft Ventricular Hypertrophy  IDA  RGD 

Phenotype Annotations    Click to see Annotation Detail View

Mammalian Phenotype

Object SymbolSpeciesTermQualifierEvidenceWithNotesSourceOriginal Reference(s)
Cm7Ratabnormal aortic weight  QTM  RGD 
Cm8Ratabnormal aortic weight  QTM  RGD 
Cm9Ratabnormal aortic weight  QTM  RGD 
SS/JrRkbRatcardiac interstitial fibrosis  IAGP on 4% NaCl dietRGD 
Cm10Ratheart left ventricle hypertrophy  QTM  RGD 
Cm11Ratheart left ventricle hypertrophy  QTM  RGD 
Cm12Ratheart left ventricle hypertrophy  QTM  RGD 
SS/JrRkbRatincreased aortic weight  IAGP compared to SHR/FubRkb on 4% NaCl dietRGD 
SS/JrRkbRatincreased heart left ventricle weight  IAGP compared to SHR/FubRkb on 4% NaCl dietRGD 
Bp108Ratincreased systemic arterial blood pressure  QTM  RGD 
SS/JrRkbRatincreased systemic arterial blood pressure  IAGP compared 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