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Sudden infant death syndrome (SIDS) is associated with serotonin (5-HT) neuron abnormalities. There is evidence of autonomic dysfunction during sleep in infants eventually succumbing to SIDS, as well as cardiovascular collapse before death. Neonatal rodents deficient in central 5-HT display hypotension and bradycardia. We hypothesized that central 5-HT reduces cardiac vagal tone and increases sympathetic vascular tone and, given the firing pattern of 5-HT neurons, that these effects are greater in quiet sleep (QS) than in active sleep (AS). We tested these hypotheses using 2-wk-old male and female rat pups lacking tryptophan hydroxylase-2 ( TPH2 −/− ) and wild-type (WT) littermates. Arterial blood pressure (ABP) and heart rate (HR) were measured over 3 h during periods of QS and AS. We also gave atropine or atenolol (each 1 mg/kg iv), or phentolamine (5, 50, and 500 μg/kg iv) to separate groups to assess the effects 5-HT deficiency on autonomic tone to the heart or sympathetic vascular tone, respectively. Compared with WT, male and female TPH2 −/−  pups had reduced ABP in QS but not in AS. Atropine induced a greater HR increase in female TPH2 −/−  than in female WT pups, an effect absent in male TPH2 −/−  pups. Both genotypes experienced the same atenolol-induced drop in HR. In males only, phentolamine induced a smaller decrease in the ABP of TPH2 −/−  pups compared with WT. These data suggest that central 5-HT maintains ABP in QS, and HR in both states. In males, central 5-HT facilitates sympathetic vascular tone, and in females it reduces cardiac vagal drive.

american journal of physiology. regulatory, integrative and comparative physiology/american journal of physiology. regulatory, integrative, and comparative physiology

Central serotonin and the control of arterial blood pressure and heart rate in infant rats: influence of sleep state and sex