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

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.