Low affinity nerve growth factor receptor gene co-segregates with decreased bodyweight and increased left ventricular weight in spontaneously hypertensive rats

1. The sympathetic nervous system influences the cardiovascular and hormonal systems and sympathetic innervation is dependent on nerve growth factor (NGF). The NGF gene is linked genetically to high blood pressure in the spontaneously hypertensive rat (SHR) and there exists a mutation in the SHR low...

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Vydáno v:Clinical and experimental pharmacology & physiology Ročník 23; číslo 6-7; s. 614
Hlavní autoři: Kapuscinski, M K, Nemoto, K, Ueyama, T, Charchar, F, Kageyama, H, Fukumachi, K, Sekimoto, M, Senba, E, Tomita, T, Tomita, I, Harrap, S B
Médium: Journal Article
Jazyk:angličtina
Vydáno: Australia 01.07.1996
Témata:
Alleles
Animals
Blood Pressure - drug effects
Blood Pressure - physiology
Body Weight - genetics
DNA - analysis
DNA Primers
Female
Hypertension - genetics
Hypertension - metabolism
Hypertension - pathology
Hypertrophy, Left Ventricular - genetics
Hypertrophy, Left Ventricular - metabolism
Hypertrophy, Left Ventricular - pathology
Male
Mutation
Phenotype
Rats
Rats, Inbred SHR
Receptors, Nerve Growth Factor - genetics
ISSN:0305-1870
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Popis
Shrnutí:1. The sympathetic nervous system influences the cardiovascular and hormonal systems and sympathetic innervation is dependent on nerve growth factor (NGF). The NGF gene is linked genetically to high blood pressure in the spontaneously hypertensive rat (SHR) and there exists a mutation in the SHR low affinity NGF receptor (LNGFR) gene. 2. To determine whether the LNGFR mutation was linked genetically with cardiovascular phenotypes we studied an F2 population derived from SHR and normotensive Donryu (DRY) rats. 3. Mean arterial pressure (MAP), left ventricular mass (LVM) and related phenotypes were measured in 127 20 week old male F2 rats and correlated with the inheritance of the SHR mutation (S) and/or the DRY allele (D) of the LNGFR. 4. Analysis of variance revealed that the S mutation was associated with a significantly lower bodyweight in F2 rats (P < 0.0001). 5. The S mutation was associated with a significant (P < 0.007) increase in LVM:bodyweight ratio, but not with differences in right ventricular or kidney weights corrected for bodyweight. We found no association between MAP and LNGFR alleles or genotypes. 6. These results suggest that the mutation in the signal peptide of LNGFR may serve as a useful marker for the analysis of genetic factor(s) involved in the differential determination of body size and heart weight.
Bibliografie:ObjectType-Article-1
SourceType-Scholarly Journals-1
ObjectType-Feature-2
content type line 23
ISSN:0305-1870
DOI:10.1111/j.1440-1681.1996.tb02797.x