Atenolol Enhances Growth Hormone Release to Exogenous Growth Hormone-Releasing Hormone but Fails to Alter Spontaneous Nocturnal Growth Hormone Secretion in Boys with Constitutional Delay of Growth

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Abstract
We tested the hypothesis that selective β1-adrenergic blockade will enhance growth hormone (GH) secretion in boys with constitutional delay of growth in response to both exogenously administered growth hormone-releasing hormone as well as to endogenous GH-releasing hormone pulsations. The study group comprised eight healthy, short, prepubertal boys ranging from 7 2/12 to 15 0/12 yr old with bone ages delayed 15 to 42 months. All had demonstrated GH levels of greater than 10 ng/ml following a pharmacologic or physiologic stimulus. During two consecutive nights, blood samples were withdrawn every 20 min for GH determination between 2000 and 0800 h. Immediately after each 0800 h blood withdrawal, 1 μg/kg of GH-releasing hormone (1–40)-OH was administered intravenously to each subject and blood was withdrawn every 15 min for an additional 2 h. During the day before the second overnight sampling period each subject received atenolol, 25 mg orally, at 1030 and 1600 h to induce β-adrenergic blockage. The six subjects in whom β-adrenergic blockade could be documented had enhanced GH release after GH-releasing hormone administration on the atenolol treatment day both in terms of higher peak GH levels achieved p < 0.05) as well as greater total GH secretion (3916 ± 701 versus 5624 ± 986 ng/ml min, p < 0.01). In contrast, there were no differences in endogenous, unstimulated nocturnal GH pulse characteristics between study and control days. In particular, there were no changes in number of GH pulses, mean 12-h GH concentrations, mean GH pulse height, amount of GH secreted in pulses, mean interpulse GH levels, or total area under the GH versus time curve.

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