Key result
Introgression of chromosome 13 in SS.BN13 rats restored arteriolar dilator responses to acetylcholine regardless of elevated salt intake, compared to impaired dilation in Dahl S rats on a high salt diet.
Why the study?
Does introgression of chromosome 13 from the normotensive Brown Norway strain prevent altered arteriolar reactivity to vasoactive stimuli in Dahl salt-sensitive rats on a high salt diet?
Population
Dahl salt-sensitive (S) rats and consomic SS.BN13 rats
Comparison
High salt diet (4%) for 4 to 6 days or 4 weeks vs Low salt diet (0.4%) for 4 to 6 days or 4 weeks
Design
Preclinical
Follow-up
4 to 6 days or 4 weeks
Authors
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Rat model data on chromosome 13 should not alter hypertension care; leaves open whether renin gene variants modulate salt sensitivity in humans.
Does introgression of chromosome 13 from the normotensive Brown Norway strain prevent altered arteriolar reactivity to vasoactive stimuli in Dahl salt-sensitive rats on a high salt diet?
Restitution of normal renin control mechanisms by chromosomal transfer restores dilator responses in salt-sensitive rats, suggesting a genetic basis for vascular reactivity independent of blood pressure.
Drenjančević et al. (2003) studied Vascular reactivity / Salt-sensitive hypertension. Introgression of chromosome 13 (SS.BN13 consomic rats) and high salt diet vs. Dahl S rats and low salt diet (0.4%) was evaluated on Arteriolar responses to elevated superfusion solution PO2, acetylcholine, and sodium nitroprusside. Introgression of chromosome 13 in SS.BN13 rats restored arteriolar dilator responses to acetylcholine regardless of elevated salt intake, compared to impaired dilation in Dahl S rats on a high salt diet.
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