Dopaminergic Regulation of Growth Hormone (GH) Secretion in Normal Man: Correlationof L-Dopa and Dopamine Levels with the GH Response*

Although it is clear that dopamine (DA) can affect PRL and GH release at the level ofthe hypothalamus and median eminence⁄pituitary gland, the relative importance of the site of control remains unclear. Consequently, we differentially altered central or peripheral DA levelsby administering L-dopa (250 mg) orally to six healthy male volunteers after pretreatment with theperipheral decarboxylase inhibitor carbidopa (central action), iv DA (4 µg⁄kg-min,peripheral action),and L-dopa (500 mg orally, both central and peripheral actions). The changes inGHand PRL observed were correlated with the concentrations of L-dopa and DA measured by the radioenzymatic technique. Peak L-dopa and DA levels were 1.2 ± 0.3 jug⁄ml and 8.4 ± 1.9 ng⁄ml after L-dopa and 2.5 ± 0.6 jug⁄ml and 1.7 ± 0.5 ng⁄ml, respectively, when half the L-dopa dose was combined with carbidopa. While DA and L-dopa concentrations were significantly correlated after L-dopa (r = 0.9), this relationship was abolished by carbidopa.Peak GH levels were comparable after both drug regimens, but the GH response correlated with L-dopa (r = 0.85) or DA (r = 0.70) concentrations only when L-dopa was given without carbidopa. During the infusion of DA, circulating DA levels reached 49.4 ± 5.4 ng⁄ml and GH increased to 10.4 ± 3.5 ng⁄ml. PRL concentrations fell comparably after each of the three regimens, but baseline values were significantly increased by carbidopa pretreatment, suggesting that basal PRL is modulated by circulating DA. Therefore, since treatment with carbidopa plus L-dopa has a predominant central effect, DA has a peripheral effect, and L-dopa has both peripheral and central effects, our data strongly support both peripheral (pituitary and⁄or median eminence) and central modulation of GH as well as PRL secretion in normal man.