LITHIUM DOES NOT PREVENT AGONIST-INDUCED SUBSENSITIVITY OF HUMAN ADENYLATE-CYCLASE

  • 1 January 1982
    • journal article
    • research article
    • Vol. 17  (3) , 343-350
Abstract
Depressed patients (11) were treated with salbutamol, .alpha.,.beta.-2 adrenergic agonist and .beta.-2 adrenergic receptor sensitivity was evaluated before, during and after treatment. .beta.-Adrenergic receptor sensitivity was evaluated by measuring the plasma cAMP rise after an i.v. dose of salbutamol. Salbutamol treatment induced subsensitivity of the .beta.-adrenergic adenylate cyclase with a time course paralleling the antidepressant effects. Nine patients who were depressed despite treatment with Li were treated with salbutamol plus Li. Subsensitivity of the .beta.-adrenergic adenylate cyclase developed in the presence of Li to the same degree as in patients treated with salbutamol alone. These results represent the 1st human study of the theory that Li stabilizes receptor sensitivity changes. Failure of Li to prevent subsensitivity agrees with reports that Li fails to prevent imipramine-induced subsensitivity of .beta.-adrenergic receptors in rat cortex. Li stabilization of receptor sensitivity is apparently unidirectional, preventing supersensitivity but not subsensitivity.

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