Soukhova-O'Hare, Galia K., Zixi (Jack) Cheng, Andrew M. Roberts, and David Gozal. Postnatal intermittent hypoxia alters baroreflex function in adult rats. Am J Physiol Heart Circ Physiol 290: H1157-H1164, 2006. First published September 9, 2005 doi:10.1152/ajpheart.00767.2005.-Chronic perinatal intermittent hypoxia (IH) could have long-term cardiovascular effects by altering baroreflex function. To examine this hypothesis, we exposed rats (n ϭ 6/group) for postnatal days 1-30 or prenatal embryonic days 5-21 to IH (8% ambient O2 for 90 s after 90 s of 21% of O2, 12 h/day) or to normoxia (control). Baroreflex sensitivity (BRS) and cardiac chronotropic responses were examined in anesthetized animals 3.5-5 mo later by infusing phenylephrine or sodium nitroprusside (6 -12 g/min iv, 1-2 min) during normoxia and after 18 min of acute IH (IHA). In controls after IHA, baroreflex gain was 42% (P Ͻ 0.05) less than during normoxia. BRS in the postnatal IH group during normoxia was ϳ50% less than in control rats and similar to controls after IHA. The heart rate response to phenylephrine in the IH group was also less than in controls (P Ͻ 0.05) and was not changed by IHA. BRS and heart rate responses in the prenatal IH group were similar to the normoxic control group. Vagal efferent projections to atrial ganglia neurons in rats after postnatal IH (n ϭ 4) were examined by injecting tracer into the left nucleus ambiguus. After 35 days of postnatal IH, basket ending density was reduced by 17% (P Ͻ 0.001) and vagal axon varicose contacts by 56% (P Ͻ 0.001) compared with controls. We conclude that reduction of vagal efferent projections in cardiac ganglia could be a cause of long-term modifications in baroreflex function.perinatal intermittent hypoxia; vagus; atrial ganglia; basket endings RECURRENT APNEAS THAT CAUSE oxygen desaturation and bradycardia are often present in preterm infants (33). However, the long-term effects of neonatal intermittent hypoxia (IH) on cardiovascular regulation and sympathovagal balance are not well known. Adults who experience IH during sleep-disordered breathing such as obstructive sleep apnea have a high risk of developing hypertension, myocardial ischemia, and heart failure (40, 52). Sympathetic overactivity, decreased baroreflex sensitivity (BRS), and decreased heart rate variability have been found in these patients (6,30,36,37,46). In a rodent model of obstructive sleep apnea, Fletcher et al. (16) demonstrated blood pressure elevation after 30-day exposure to IH. Involvement of the sympathetic efferent arm of the arterial chemoreflex arc was suggested by prevention of the blood pressure response after pharmacological sympathetic blockade or carotid body deafferentiation (16 -19, 50). On the other hand, withdrawal of parasympathetic activity could also contribute to the alteration of sympathovagal balance observed in obstructive sleep apnea, as shown by power spectrum analysis of heart rate variability (26,35,55).Perinatal susceptibility to hypoxia is characterized by the developmental window...