Long-term regulatory mechanisms for tyrosine hydroxylase in sympathetic ganglia and carotid body.

The delayed activation of TH elicited by hypoxia in carotid body indirectly suggests that the release of dopamine is part of the responses elicited by hypoxia. The TH activation appears to be independent from nicotinic receptor stimulation and can be abolished by dopaminergic receptor stimulation. Dexamethasone also increases the activity of TH. Since both hypoxia and dexamethasone fail to change the kinetic constants, the long-term increase of TH could be viewed as an expression of new synthesis of enzyme molecules. This assumption is supported by the evidence presented on the prompt kinetic change in PDE, which according to the model proposed by Uzunov et al. (42) expresses the participation of a prompt and sustained response of the second messenger in postsynaptic cells. It remains to be ascertained whether the change in the catalytic activity of PDE which metabolizes the second messenger can be suppressed by dopamine-receptor blockers. Immediate changes of PDE coupled with the delayed increase in TH activity may contribute to a better understanding of the neuronal mechanisms controlling the chemoreceptor function. It is hoped that the continuation of these studies will help to define the function of type I cells in the carotid body.