Heterozygous Knock-Out of ET B Receptors Induces BQ-123–Sensitive Hypertension in the Mouse
Population
Mice with heterozygous knock-out of ET(A) or ET(B) receptors and wild-type littermates
Comparison
Heterozygous knock-out of ET receptors… vs Wild-type littermates and ET knock-out mice
Design
Preclinical
Authors
Discussion
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Implication
ET(B) haploinsufficiency elevates blood pressure via unopposed ET(A) signaling in mice; leaves open whether ET(A) antagonists merit human hypertension trials.
Structured PICO
P
Population
Mice with heterozygous knock-out of ET(A) or ET(B) receptors and wild-type littermates
I
Intervention
Heterozygous knock-out of ET(B) receptors; administration of exogenous endothelin-1 (ET-1), IRL-1620 (ET(B) agonist), BQ-123 (ET(A) antagonist), or BQ-788 (ET(B) antagonist)
C
Comparator
Wild-type littermates and ET(A) (+/-) knock-out mice
O
Outcome
Mean arterial blood pressure and pressor response to ET-1 and IRL-1620surrogate
Heterozygous knock-out of ET(B) receptors in mice induces a hypertensive state that is sensitive to ET(A) antagonism, suggesting ET(B) receptors play a key physiological role in opposing endogenous ET-1-dependent pressor effects.
Cite This Study
Berthiaume et al. (2000) studied this question.