Key result
ET(B) receptor-deficient rats exhibited earlier and higher increases in systolic blood pressure and more severe renal and vascular damage in response to DOCA-salt than wild-type rats.
Why the study?
Does ABT-627 reduce DOCA-salt-induced hypertension and tissue injury in ET(B) receptor-deficient rats?
Population
Transgenic spotting-lethal rats with ET receptor deficiency (rescued with DssH-ET transgene) and wild-type…
Comparison
ABT-627 (ET receptor antagonist) chronic treatment vs Wild-type rats and/or no ABT-627 treatment
Design
Preclinical
Authors
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ET(B) receptor protection against salt-induced hypertension is reinforced in this rat model; leaves open translation to human disease.
Does ABT-627 reduce DOCA-salt-induced hypertension and tissue injury in ET(B) receptor-deficient rats?
ET(B) receptors play a protective role in DOCA-salt-induced hypertension, and ET(A) receptor antagonism with ABT-627 prevents hypertension and tissue injury in this model.
Matsumura et al. (2000) studied DOCA-salt-induced hypertension. ET(B) receptor deficiency vs. Wild-type (+/+) rats was evaluated on Systolic blood pressure, renal dysfunction, and vascular hypertrophy. ET(B) receptor-deficient rats exhibited earlier and higher increases in systolic blood pressure and more severe renal and vascular damage in response to DOCA-salt than wild-type rats.
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