Hormone action at the membrane level. VII. Stimulation of dihydroalprenolol binding to beta-adrenergic receptors in isolated rat heart ventricle slices by triiodothyronine and thyroxine.

Thyroxine (T4) and triiodothyronine (T3) increase the number of beta-adrenergic receptors in heart ventricle slices. A short term effect reaches a maximum by 1.5-2 h and requires added amino acids for consistent results. The apparent Km for the L-T3 effect is 15 pM. This effect, measured by an increase in stereospecific binding of (-)-[3H]dihydroalprenolol is not inhibited by cycloheximide or puromycin and is produced more effectively by L-T3 than D-T3. However, cycloheximide nearly completely inhibits protein synthesis in the 2-3 h incubation time. T3 also gives a small inhibition of protein synthesis during this time interval. The early effect of T3 stimulation of dihydroalprenolol binding is considered to be a post-translational event shereby T3 enhances the transport of existing beta-adrenergic receptors from the cytosol into the membrane. A long term (15 h) stimulation of dihydroalprenolol binding to ventricle membranes is also produced by L-T3. This effect is stereospecific, is inhibited by cycloheximide, and is believed to be a transcriptional-translational event leading to the synthesis of new beta-adrenergic receptors by T3.