Impaired control of renal sympathetic nerve activity following neonatal intermittent hypoxia in rats

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, 12 h/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 μg/min/100 g) and sodium nitroprusside (SNP, 1.5 μg/min/100 g). 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.