Neonatal hyperthyroidism causes premature development of baroreceptor-mediated cardiac sympathetic reflexes.

Baroreceptor-mediated reflex control of cardiac sympathetic activity does not appear fully until the third week of postnatal age in the rat, possibly because central processing of baroreceptor sensory input is deficient in the neonate. Hyperthyroidism, which accelerates synaptogenesis in the peripheral sympathetic and central nervous systems, was produced by administering 3,3',5-triiodothyronine (T3) daily, and effects on development of baroreceptor-mediated sympathetic reflexes were evaluated. To test baroreceptor-mediated reflexes, control and T3-treated rats of different ages were given hydralazine acutely to produce a decrease in blood pressure, which in adult rats results in a large, sympathetically-mediated stimulation of cardiac ornithine decarboxylase (ODC) activity. In control neonates, cardiac ODC responses to hydralazine were absent until the 3rd week of age, but the T3-treated animals showed increases as early as 8 days of age. Furthermore, increased turnover of norepinephrine in cardiac sympathetic nerves in response to the hydralazine-induced hypotension was 2- to 3-fold higher in the 8-day-old T3-treated animals than in controls. These data indicate that the early appearance of the ODC response to hypotension in hyperthyroid rats results, at least in part, from precocious development of the ability of baroreceptor input to influence efferent sympathetic function.