Effect of Adrenergic Stimulation and Blockade on Melatonin Secretion in the Human

Abstract

The mechanisms that control release of melatonin from the human pineal gland are unknown. This chapter mentions experimental data in animals which are relevant to the present study in humans. It has been established in animals, that the pineal gland is innervated by post-ganghonic fibers from the superior cervical ganglia, which secrete the neurotransmitter noreprinephrine. The presence of β -adrenergic receptors on pineal cell membranes has been demonstrated by the ability of β -adrenergic receptor antagonists to competitively inhibit norepinephrine-induced actions in pinealocyte metabolism. Among the more important of these actions are the activation of adenyl cyclase and the induction of N-acetyl transferase activity, resulting eventually in increased melatonin synthesis. The ability of pharmacologic p-agonists such as isoproterenol to produce an increase of N-acetyl transferase activity, and of &blockers such as propanolol to inhibit it, confirms that, in the rat, melatonin synthesis and presumably release, are mediated by a β -adrenergic system. Further, the sensitivity of these receptors to stimulation appears to vary inversely with the extent of previous stimulation. In addition to a β -adrenergic system, there is some evidence of a dopaminergic influence on melatonin synthesis, as dopamine increases melatonin production in organ culture. In addition, L-dopa increases rat pineal melatonin concentration and N-acetyl transferase activity.