Reverse tri-iodothyronine as part of alpha 2 adrenergic receptors.
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 (rT3) levels are also low in hypothyroidism and levels are high in hyperthyroidism induced by T4 administration. The present author has proposed that rT3 is incorporated into the alpha 2 adrenergic receptor where it provides the aromatic binding site. Tri-iodothyronine (T3) administration does not raise alpha 2 adrenergic receptor numbers above normal control values. This is consistent with the author's hypothesis as T3 cannot be converted to rT3. This paper describes how rT3 could provide the aromatic binding site for drugs that act on alpha 2 adrenergic receptors.
D000316:Adrenergic alpha-Agonists / Q000378:metabolism; D000317:Adrenergic alpha-Antagonists / Q000378:metabolism; D001665:Binding Sites; D008968:Molecular Conformation; D011942:Receptors, Adrenergic, alpha / Q000032:analysis / Q000378:metabolism*; D014285:Triiodothyronine, Reverse / Q000378:metabolism*; D015016:Yohimbine / Q000378:metabolism
D000316:Adrenergic alpha-Agonists; D000317:Adrenergic alpha-Antagonists; D011942:Receptors, Adrenergic, alpha; D015016:Yohimbine; D014285:Triiodothyronine, Reverse