Key result
In salt-sensitive Dahl rats on a high-sodium diet, ET(A) receptor antagonist LU135252 partially reduced systolic blood pressure (168 vs 190 mm Hg, P<0.05) and normalized vascular reactivity.
Why the study?
Does ET(A) receptor antagonist LU135252 prevent vascular dysfunction and aortic hypertrophy in salt-sensitive Dahl rats on a high-sodium diet?
Population
Salt-sensitive (DS) and salt-resistant (DR) Dahl rats
Comparison
ET receptor antagonist LU135252 added to a… vs High-sodium diet (NaCl 4%) without LU135252
Design
Preclinical
Follow-up
two months
Authors
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Hypothesis-generating for ET(A) antagonism in salt-sensitive hypertension; requires human trials before any clinical consideration.
Does ET(A) receptor antagonist LU135252 prevent vascular dysfunction and aortic hypertrophy in salt-sensitive Dahl rats on a high-sodium diet?
Absolute Event Rate: 168% vs 190%
p-value: p=<.05
ET(A) receptor antagonism prevents vascular dysfunction, aortic hypertrophy, and increased tissue ET-1 in a rat model of salt-sensitive hypertension.
Barton et al. (1998) studied Salt-sensitive hypertension. ET(A) receptor antagonist LU135252 vs. High-sodium diet without LU135252 was evaluated on Systolic blood pressure (p=<.05). In salt-sensitive Dahl rats on a high-sodium diet, ET(A) receptor antagonist LU135252 partially reduced systolic blood pressure (168 vs 190 mm Hg, P<0.05) and normalized vascular reactivity.
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