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Atenolol Enhances Nocturnal Growth Hormone (GH) Release in GH-Deficient Children during Long Term GH-Releasing Hormone Therapy^*

PAUL M. MARTHA, JR., ROBERT M. BLIZZARD, MICHAEL O. THORNER and ALAN D. ROGOL

Departments of Pediatrics (P.M., R.M.B., A.D.R.), Internal Medicine (M.O.T.), and Pharmacology (A.D.R.), University of Virginia Health Sciences Center Charlottesville, Virginia 22908

Address all correspondence and requests for reprints to: Alan D. Rogol, M.D., Ph.D., Department of Pediatrics, MR-4/Room 3037, University of Virginia Health Sciences Center, Charlottesville, Virginia 22908.

The effect of the selective ft-adrenergic blocking agent atenolol (50 or 100 mg, orally) on spontaneous and GHreleasing hormone (GHRH)-stimulated GH release was evaluated in six GH-deficient children during long term therapy with GHRH. Nocturnal GH concentrations were determined every 20 min for 12 h under the following four conditions: 1) control, 2) atenolol administration only, 3) sc GHRH administration only, and 4) combined GHRH and atenolol administration.

The mean 12-h nocturnal GH concentrations after administration of atenolol alone [2.4 ± 0.6 µg/L (mean ± SEM)] or GHRH alone (2.7 ± 1.0 µg/L) were indistinguishable from baseline values (2.0 ± 0.5 /µg/L; P > 0.05). In contrast, the addition of atenolol to ongoing GHRH therapy caused a clear augmentation of 12-h overnight GH release compared to that during all other study periods (5.0 ± 1.3 µg/L; P < 0.05). In a subset of three subjects for whom GH pulse characteristics were determined, the primary mode of the enhanced GH release was through an increase in the amplitude of serum GH pulses.

These results are consistent with the hypothesis that β-adrenergic blocking compounds enhance the responsivity of the pituitary gland to agents that permit GH release by inhibiting hypothalamic somatostatin secretion or action. They suggest that atenolol may have potential as an adjunctive therapy in some children with abnormalities of GH secretion when GHRH is the primary therapeutic agent.

^* Presented in part at the Annual Meeting of the American Pediatric Society, Anaheim, CA, 1987. This work was supported in part by a grant from the USPHS (General Clinical Research Centers) at the University of Virginia (RR-00847) and Grants DK-32632 (to M.O.T.) and AG-04303 (to R.M.B.).

Recipient of a Clinical Investigator Award (HD-00868) from the NICHHD.

Received July 6, 1989.