Key result
In isolated beating rabbit atria, acute hypoxia significantly promoted ET-1 production, which regulated ANP secretion through the activation of ET receptors and the MAPK/ERK and PI3K/Akt signaling pathways.
Why the study?
Does endogenous ET-1 regulate hypoxia-induced ANP secretion via MAPK/ERK and PI3K/Akt pathways in isolated rabbit atria?
Population
Isolated perfused beating left atria from adult New Zealand white rabbits of either sex
Comparison
Acute hypoxia with or without ET receptor… vs Normoxic control with vehicle
Design
Preclinical, randomly divided
Follow-up
Acute experiment (minutes)
Authors
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Does not inform clinical practice; leaves open ET-1/ANP pathway relevance in human hypoxia or heart disease.
Does endogenous ET-1 regulate hypoxia-induced ANP secretion via MAPK/ERK and PI3K/Akt pathways in isolated rabbit atria?
p-value: p=<0.001
Acute hypoxia promotes atrial ET-1 production, which regulates ANP secretion through ET receptors and the MAPK/ERK and PI3K/Akt signaling pathways.
Bian et al. (2016) studied Hypoxia-induced Atrial Natriuretic Peptide (ANP) secretion (n=86). ET receptor antagonists (BQ123, BQ788) and signaling inhibitors (PD098059, LY294002) vs. Hypoxia alone and normoxic control was evaluated on Hypoxia-induced ANP secretion (p=<0.001). In isolated beating rabbit atria, acute hypoxia significantly promoted ET-1 production, which regulated ANP secretion through the activation of ET receptors and the MAPK/ERK and PI3K/Akt signaling pathways.
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