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Do -Adrenergic Mechanisms Regulate Spontaneous or Opiate-Modulated Pulsatile Luteinizing Hormone Secretion in Man?^*

Division of Endocrinology, Departments of Internal Medicine, Virginia School of Medicine Charlottesuille, Virginia 22908
Division of Endocrinology, Departments of Pharmacology and Pediatrics, Virginia School of Medicine Charlottesuille, Virginia 22908
The Biomathematics Section, Department of Pharmacology, University of Virginia School of Medicine Charlottesuille, Virginia 22908

Address requests for reprints to: Dr. Johannes D. Veldhuis, Department of Medicine, Box 202, Division of Endocrinology, University of Virginia School of Medicine, Charlottesville, Virginia 22908.

Brain noradrenergic mechanisms participate in the excitatory control of episodic LH release in many experimental animals, including the nonhuman primate. In addition, augmentation of pulsatile LH release in the rodent in response to opiate receptor antagonists is dependent upon intact central noradrenergic pathways. The applicability of these tenets to humans is not known. We tested the excitatory influence of brain noradrenergic systems on pulsatile LH secretion in normal men by administering phenoxybenzamine (an irreversible, preferentially postsynaptic, ₁-receptor blocker) or -methyldopa (an inhibitor of brain adrenergic transmission). Five normal men underwent repetitive (every 20 min) venous sampling for 8 h to characterize episodic LH release quantitatively under basal conditions and after the administration of naltrexone, a potent opiate receptor antagonist which stimulates puslatile LH release. Subjects received saline, phenoxybenzamine (1 mg/kg, iv, over 90 min), or -methyldopa (250 mg, orally, every 6 h). The following parameters of spontaneous episodic LH secretion were not altered after phenoxybenzamine or -methyldopa administration: mean and integrated serum LH concentrations, LH pulse frequency, LH pulse amplitude (percentage or milliinternational units per ml increment), and absolute peak serum LH values. In addition, the administration of adrenergic inhibitors did not impede the capacity of naltrexone to significantly augment pulsatile LH secretion in these subjects. We conclude that in the doses used, phenoxybenzamine and -methyldopa do not alter spontaneous or opiate-modulated episodic LH release in normal men.

^* This work was supported by Research Career Development Award AM-00153 (to A.D.R.), NIH Biomedical Research Support Award 5S07-RR-05431, NIDA Grant R03-DA-03315-01, a University of Virginia Computer Services Grant (to J.D.V.), USPHS General Clinical Research Grant RR-847, and Diabetes Research and Training Center Grant 5-P60-AM-22125-05.

Received May 4, 1983.