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Prenatal hypoxia programs changes in β-adrenergic signaling and postnatal cardiac contractile dysfunction.
1AVIAN Behavioural Genomics and Physiology, IFM Biology, Linköping University, Linköping, Sweden.
Summary
Prenatal hypoxia in chickens caused heart changes and systolic dysfunction by 5 weeks. This suggests downstream calcium handling, not beta-adrenergic receptors, impacts cardiac contractility.
Area of Science:
- Cardiovascular Physiology
- Developmental Biology
- Environmental Health
Background:
- Prenatal hypoxia is a risk factor for adult cardiovascular disease.
- Previous studies show prenatal hypoxia programs cardiac beta-adrenergic receptor (βAR) response.
Purpose of the Study:
- Investigate if reduced βAR sensitivity in prenatally hypoxic chicken hearts links to β1AR/β2AR, Gαi changes, and cAMP accumulation.
- Determine the in vivo effect of prenatal hypoxia on heart function.
Main Methods:
- Eggs incubated in normoxia or hypoxia (14% O2) from day 0.
- Assessed cardiac β1AR/β2ARs, Gαs/Gαi proteins, and cAMP accumulation.
- Evaluated in vivo heart function using echocardiograms and collagen content via tissue staining.
Main Results:
- Prenatally hypoxic hearts showed increased relative heart mass, β1ARs, and Gαs.
- No significant changes in cAMP or collagen content.
- Echocardiograms revealed systolic contractile dysfunction in hypoxic group.
Conclusions:
- Prenatal hypoxia induces cardiac hypertrophy and systolic dysfunction in young chickens.
- Observed βAR and G protein changes may represent an early compensatory stage.
- Downstream Ca(2+) handling, not proximal βAR system changes, likely causes decreased cardiac contractility.
