Key result
High-salt diet progressively increases SBP and induces arterial dysfunction in diverse mice.
Why the study?
Excess salt consumption contributes to hypertension and arterial dysfunction in humans, but this phenotype is not observed in inbred, genetically identical mice fed a high-salt diet.
Does a high-salt diet increase systolic blood pressure and induce arterial dysfunction in outbred, genetically diverse mice?
Does a high-salt diet increase systolic blood pressure and induce arterial dysfunction in outbred, genetically diverse mice?
A high-salt diet in outbred, genetically diverse mice progressively increases systolic blood pressure and induces arterial dysfunction, providing a translational model for human salt-induced hypertension.
Answers are grounded in this paper and cite their sources.
May support salt reduction counseling; extends rodent models to genetically diverse strains but leaves translation open.
Excess salt consumption is a contributor to hypertension and arterial dysfunction in humans living in industrialized societies, but this phenotype is not observed in inbred, genetically identical mice that consume a high-salt (HS) diet. This study reveals that a HS diet in outbred, genetically diverse mice progressively increases systolic blood pressure and induce arterial dysfunction. These data suggest that genetically diverse mice may provide translational insight into arterial adaptations in humans that consume an HS diet.
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Zheng et al. (2023) studied Hypertension and arterial dysfunction. High-salt (HS) diet was evaluated on Systolic blood pressure and arterial dysfunction. A high-salt diet in outbred, genetically diverse mice progressively increases systolic blood pressure and induces arterial dysfunction.
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