Dopamine Inhibition of Stimulated Growth Hormone Secretion: Evidence for Dopaminergic Modulation of Insulin- and L-Dopa-Induced Growth Hormone Secretion in Man*

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Abstract
Previous studies have shown that the infusion of dopamine (DA; 4 µg/kg-min) both stimulates GH secretion and abolishes the GH response to hypoglycemia when insulin (0.1 U/kg) is given 30 min after the start of the infusion. Additional studies on the mechanism of this inhibitory effect are now reported. When insulin was given to seven normal male volunteers 15 min before the start of the DA infusion, the maximal GH increment (44.7 ± 5.7 ng/ml) was comparable to insulin alone (45.5 ± 5.3 ng/ml), and both were greater than the maximum increment when insulin was given 30 or 120 min into the DA infusion (17.3 ± 3.3 and 23.0 ± 7.4 ng/ml, respectively; P < 0.05). In contrast, DA potently inhibited PRL secretion regardless of the timing of DA and insulin; PRL fell during all DA plus insulin studies despite a maximal PRL increment after insulin alone of 24.4 ± 6.0 ng/ml. The GH response to 500 mg L-dopa given orally was inhibited by DA in a fashion similar to the insulin response. Thus, when L-dopa was given to six men 30 min into DA infusion, GH levels rose early and returned to baseline by the end of the study in a pattern similar to DA alone. Therefore, the late and sustained GH responses that were observed during L-dopa alone were completely abolished. Despite the similarity in time course and magnitude of the GH responses to DA and arginine, prior arginine infusion did not affect the GH response to subsequent insulin hypoglycemia. When insulin was given to five healthy men at the end of a 30-min arginine infusion (30 g), GH levels were comparable to the summation of the individual responses and the maximal GH increments were similar [arginine plus insulin, 29.8 ± 3.2 (SE); insulin alone, 40.3 ± 5.2 ng/ml; P = NS] We conclude from these data that DA inhibits GH release stimulated by L-dopa and insulin; the DA inhibition of insulinstimulated GH, but not PRL, release requires a critical latency interval. Failure of arginine to inhibit insulin-induced GH release indicates that the inhibitory effects of DA are not due simply to prior GH secretion. DA inhibition of GH secretion may be specific for DA-mediated GH secretion, providing inferential evidence for a dopaminergic mechanism in hypoglycemia-mediated GH secretion.

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