Abstract
Thyroid hormones affect alpha and beta adrenergic receptor number profoundly. Presynaptic and post synaptic alpha 2 adrenergic receptor number is decreased in hypothyroidism. Behavioural studies show decreased presynaptic alpha 2 adrenergic function in hypothyroidism and increased function in hyperthyroidism. Reverse tri-iodothyronine (rT 3) lelels are also low in hypothyroidism and levels are high in hyperthyroidism induced by T 4 administration. The present author has proposed that rT 3 is incorporated into the alpha 2 adrenergic receptor where it provides the aromatic binding site. Tri-iodothyronine (T 3) administration does not raise alpha 2 adrenergic receptor numbers above normal control values. (5) This is consistent with the author's hypothesis as T 3 cannot be converted to rT 3. This paper describes how rT 3 could provide the aromatic binding site for drugs that act on alpha 2 adrenergic receptors.
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