Impaired control of renal sympathetic nerve activity following neonatal intermittent hypoxia in rats
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Updated: Aug 11, 2026
The Hypoxic Ischemic Encephalopathy Model of Perinatal Ischemia
Published on: November 19, 2008
Galia K Soukhova-O'Hare1, Andrew M Roberts, David Gozal
1Department of Pediatrics, Kosair Children's Hospital Research Institute, University of Louisville, Louisville, KY 40202, USA. gohare@aecom.yu.edu
Insights
Neonatal intermittent hypoxia in rats leads to long-term problems with how the body controls blood pressure and heart rate. This impaired baroreflex control may affect sympathetic nerve activity later in life.
Area of Science:
- Physiology
- Neonatal Research
- Cardiovascular Regulation
Background:
- Infants born prematurely often experience apneas and oxygen desaturations.
- Neonatal intermittent hypoxia (NIH) may have lasting effects on physiological regulation.
- Baroreflex control is crucial for maintaining cardiovascular stability.
Purpose of the Study:
- To investigate the long-term impact of chronic intermittent hypoxia (CIH) during the neonatal period on baroreflex control of sympathetic nerve activity in adult rats.
- To assess how NIH affects the sympathetic nerve response to acute intermittent hypoxia (AIH) and baroreceptor stimulation.
Main Methods:
- Sprague-Dawley rats were exposed to CIH (8% O2 for 90s alternating with 90s 21% O2, 12h/day) for the first 30 postnatal days or maintained in normoxia (controls).
- In adult rats, baseline cardiovascular parameters and plasma catecholamines were measured.
- Baroreflex sensitivity was evaluated by measuring changes in renal sympathetic nerve activity (RSNA) in response to phenylephrine and sodium nitroprusside infusions.
Main Results:
- Adult rats exposed to neonatal CIH showed significantly more frequent elevations in RSNA during AIH compared to controls.
- The gain of the sympatho-excitatory baroreflex response to AIH increased in control rats but remained unchanged in CIH-exposed rats.
- Sympatho-inhibitory responses to phenylephrine were similar in both groups and unaffected by AIH.
Conclusions:
- Postnatal intermittent hypoxia induces a long-lasting impairment in the baroreflex control of renal sympathetic nerve activity.
- These findings suggest that NIH can disrupt the normal regulation of cardiovascular function through both chemoreceptor and baroreceptor pathways.
- The study highlights potential long-term consequences of neonatal respiratory disturbances on autonomic nervous system regulation.
Abstract:
Apneas and recurring oxygen desaturations can occur in preterm infants and young children. To investigate long-term effects of neonatal intermittent hypoxia on baroreflex control of sympathetic nerve activity, we studied 5-7-month-old (adult) Sprague-Dawley rats exposed to chronic intermittent hypoxia (CIH, n=9; 8% O2 for 90 s alternating with 90 s 21% O2, 12h/day) for their first 30 postnatal days or controls exposed to normoxia (C, n=9). In adult CIH and C rats, baseline heart rate, mean arterial pressure, and plasma concentration of epinephrine and norepinephrine were similar. Baroreflex sensitivity was evaluated in anesthetized rats by changes in renal sympathetic nerve activity (RSNA) in response to i.v. infusions of phenylephrine (PE,1.5 microg/min/100g) and sodium nitroprusside (SNP, 1.5 microg/min/100g). Acute intermittent hypoxia (AIH, 18 min) induced elevations in RSNA by over 30% of baseline about three times more often in the CIH group than in the C group. After AIH, the gain of the baroreflex sympatho-excitatory response increased by approximately two times in C and did not change in CIH rats. The gain of sympatho-inhibitory responses to SNP at the maximum decrease in MAP was similar in the two groups in normoxia and was not affected by AIH. We conclude that postnatal intermittent hypoxia causes long-lasting impairment in chemoreceptor and baroreceptor control of renal nerve activity.
