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Updated: Aug 8, 2025
05:45
Delivery of In Vivo Acute Intermittent Hypoxia in Neonatal Rodents to Prime Subventricular Zone-derived Neural Progenitor Cell Cultures
Published on: November 2, 2015
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Sympathetic dysregulation induced by postnatal intermittent hypoxia
Marlusa Karlen-Amarante1, Isabela P Leirão1, Pedro L Katayama1
1Department of Physiology and Pathology, School of Dentistry, São Paulo State University, Araraquara, SP, Brazil.
Sleep
|March 3, 2023
Summary
Postnatal chronic intermittent hypoxia (pCIH) permanently increases sympathetic nerve activity, leading to higher blood pressure and cardiovascular disease risk in adulthood. This study reveals mechanisms involving enhanced neuronal firing and HIF-1α expression.
Area of Science:
- Cardiovascular Physiology
- Neuroscience
- Developmental Biology
Background:
- Postnatal chronic intermittent hypoxia (pCIH), mimicking sleep-disordered breathing, is a known risk factor for adult cardiorespiratory diseases.
- pCIH exposure in early life can lead to persistent respiratory instability and motor dysfunction into adulthood.
Purpose of the Study:
- To investigate the long-term impact of pCIH on sympathetic control of arterial pressure in rats.
- To elucidate the underlying mechanisms contributing to persistent sympathetic dysregulation.
Main Methods:
- Neonate rats were exposed to pCIH or normoxia.
- Arterial pressure and sympathetic activity were assessed in freely behaving and decerebrated adult rats.
- Neuronal firing frequency and gene expression (HIF-1α) in presympathetic neurons were analyzed.
Main Results:
- Adult pCIH rats exhibited higher baseline arterial pressure and sympathetic variability.
- Increased thoracic sympathetic nerve activity and ventromedullary presympathetic neuron firing frequency were observed in juvenile pCIH rats.
- Elevated HIF-1α mRNA expression was found in catecholaminergic presympathetic neurons of pCIH rats, persisting into older age.
Conclusions:
- pCIH enhances vasoconstrictor sympathetic drive through increased neuronal firing and HIF-1α expression.
- This persistent sympathetic overactivity contributes to elevated blood pressure and cardiovascular disease risk in adulthood.
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