Key result
Serca II gene substitution attenuates platelet aggregation and lowers systolic blood pressure versus SHR.
Population
Spontaneously hypertensive rats (SHR), normotensive Fischer 344 rats (F344), and their congenic strains
Comparison
Congenic substitution of the chromosomal segment… vs Progenitor spontaneously hypertensive rats (SHR)
Design
Preclinical
Authors
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Hypothesis-generating in hypertensive rat models; leaves open translational relevance to human hypertension and requires prospective validation.
A chromosomal segment including the Serca II gene locus contributes to hypertension and cardiac hypertrophy by augmenting Ca2+ signaling in spontaneously hypertensive rats.
Ohno et al. (2007) studied Hypertension. Congenic substitution of the chromosomal segment including the Serca II gene locus vs. Spontaneously hypertensive rats (SHR) was evaluated on Intracellular Ca2+ responses, platelet aggregation, systolic blood pressure, and ratio of heart weight to body weight. Heterozygous congenic rats with the Serca II gene segment had significantly attenuated intracellular Ca2+ responses, platelet aggregation, and lower systolic blood pressure compared with SHR.
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