NPR-A–Deficient Mice Show Increased Susceptibility to Hypoxia-Induced Pulmonary Hypertension
Population
Wild-type (+/+), heterozygous (+/-), and homozygous null mutant (-/-) mice for the NPR-A gene
Comparison
Exposure to acute hypoxia and chronic hypoxia… vs Wild-type mice and normal-O2 environment
Design
Preclinical
Follow-up
21 days
Authors
Discussion
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Implication
Does not support immediate clinical translation; leaves open NPR-A as a target for attenuating hypoxic pulmonary hypertension.
Structured PICO
P
Population
Wild-type (+/+), heterozygous (+/-), and homozygous null mutant (-/-) mice for the NPR-A gene
I
Intervention
Exposure to acute hypoxia and chronic hypoxia (10% O2 for 7 and 21 days), and administration of ANP, BNP, and CNP
C
Comparator
Wild-type mice and normal-O2 environment
O
Outcome
Right ventricular systolic pressure (RVSP), RV weight, and pulmonary vascular remodelingsurrogate
NPR-A mediates the vasorelaxant effect of ANP and plays an important role in attenuating the pulmonary vascular response to hypoxia in mice.
Cite This Study
Zhao et al. (1999) studied this question.