Key result
Dahl salt-sensitive rats exhibited a significantly blunted increase in urinary endothelin-1 excretion in response to a high-salt diet compared to salt-resistant rats (29.8 vs 112 pg/day).
Why the study?
Does decreased medullary production of ET-1 contribute to salt-sensitive hypertension in Dahl salt-sensitive rats?
Population
Dahl salt-sensitive (DS) rats and Dahl salt-resistant (DR) rats
Comparison
High sodium intake; chronic infusion of ET-1… vs Low sodium intake; Dahl salt-resistant (DR) rats
Design
Preclinical
Authors
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Impaired ET-1 excretion may contribute to salt-sensitive hypertension in this model; leaves open translation to human disease.
Does decreased medullary production of ET-1 contribute to salt-sensitive hypertension in Dahl salt-sensitive rats?
Absolute Event Rate: 29.8% vs 112%
p-value: p=<0.05
Decreased renal medullary production of ET-1 and reduced ET(B) receptor expression may play a key role in the development of salt-sensitive hypertension in Dahl salt-sensitive rats.
Speed et al. (2011) studied Salt-sensitive hypertension (n=51). High-salt diet (8% NaCl) vs. Low-salt diet (0.3% NaCl) and Dahl salt-resistant rats was evaluated on Urinary endothelin-1 excretion on a high-salt diet (p=<0.05). Dahl salt-sensitive rats exhibited a significantly blunted increase in urinary endothelin-1 excretion in response to a high-salt diet compared to salt-resistant rats (29.8 vs 112 pg/day).
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