RGD Reference Report - Quantitative trait loci mapping for intracellular calcium in spontaneously hypertensive rats. - Rat Genome Database

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Quantitative trait loci mapping for intracellular calcium in spontaneously hypertensive rats.

Authors: Ohno, Y  Suzuki, H  Tanase, H  Otsuka, K  Sasaki, T  Suzawa, T  Morii, T  Ando, Y  Maruyama, T  Saruta, T 
Citation: Ohno Y, etal., Am J Hypertens 2005 May;18(5 Pt 1):666-71.
RGD ID: 1547855
Pubmed: PMID:15882549   (View Abstract at PubMed)
DOI: DOI:10.1016/j.amjhyper.2004.12.001   (Journal Full-text)

BACKGROUND: Increased intracellular calcium ([Ca2+]i) in platelets is also proposed as an intermediate phenotype for hypertension in spontaneously hypertensive rats (SHR). Increased [Ca2+]i in platelets is hypothesized to contribute to atherothrombotic events. Platelet hyperactivity is frequently associated with cardiovascular disease. METHODS: In a genome scan, we performed the quantitative trait loci (QTL) mapping for [Ca2+]i in back-crossed rats derived from SHR and normotensive Fischer 344 rats, which demonstrated a single major QTL for hypertension on chromosome 1. Thrombin-stimulated [Ca2+]i in Ca2+-free and in Ca2+-containing buffers was measured in platelets using the Fura-2 method. RESULTS: Among the parental strains, systolic blood pressure and thrombin-stimulated [Ca2+]i were significantly greater in SHR than in Fischer 344 and F1 rats. The sarco(endo)plasmic reticulum Ca2+-dependent ATPase II gene locus (Serca2) between D12Mgh5 and D12Mgh6 showed the significant linkage for thrombin-stimulated [Ca2+]i in Ca2+-free and Ca2+-containing buffers. The peak logarithm of the odds scores were 3.6 and 3.3, respectively. These QTL explained 19.8% and 17.4% of the total variances, respectively. D3Mit13 and DXMgh1 showed suggestive linkage for thrombin-stimulated [Ca2+]i in Ca2+-free and in Ca2+-containing buffers, respectively. The peak logarithm of the odds scores were 2.6 and 2.1, respectively. CONCLUSIONS: A significant QTL for [Ca2+]i was mapped near Serca2 on chromosome 12, and suggestive QTL were identified near D3Mit13 and DXMgh1 in a genome scan. Genetic abnormalites in platelet [Ca2+]i may contribute to cardiovascular disease via platelet hyperactivity, independent of blood pressure elevation.

RGD Manual Disease Annotations    Click to see Annotation Detail View
TermQualifierEvidenceWithReferenceNotesSourceOriginal Reference(s)
hypertension  IDA 1547855 RGD 

Objects Annotated

QTLs
Calcic1  (Intracellular calcium level QTL 1)

Strains
F344/Snk  (NA)
SHR/Snk  (NA)


Additional Information