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 prior to 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 two week-old, male and female rat pups lacking tryptophan hydroxylase 2 (TPH2-/-) and wildtype littermates (WT). Arterial blood pressure (ABP) and HR were measured over 3 hr, during periods of QS and AS. We also gave atropine or atenolol (each 1 mg/kg i.v.), or phentolamine (5, 50 and 500 ug/kg, i.v.) to separate groups to assess the effects 5-HT deficiency on autonomic tone to the heart or sympathetic vascular tone, respectively. Compared to WT, male and female TPH2-/- pups had reduced ABP in QS, but not in AS. Atropine induced a greater HR increase in female TPH2-/- compared to 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 to 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, reduces cardiac vagal drive.

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