The Role of Biogenic Amines in the Regulation of Growth Hormone and Corticotropin Secretion in the Trained Conscious Dog*

Abstract

The regulation of GH [growth hormone] secretion in the unanesthetized dogs was evaluated by systemic administration of drugs which affect noradrenergic and dopaminergic receptors. L-Dopa produced significant increments in plasma GH, but with associated emesis and significant increases in plasma corticoids and blood pressure (BP). Apomorphine, a dopamine receptor agonist, similarly produced GH elevation only when given in emetic doses, again with increases in corticoids and BP. The dopamine receptor-blocking drug pimozide did not modify the GH or glucose response to L-dopa, although it abolished emesis and changes in BP and corticoids. Inhibition of peripheral decarboxylation of L-dopa with carbidopa completely blocked the GH and glucose responses to L-dopa. Clonidine, an .alpha. receptor agonist, produced significant secretion of GH without affecting BP or the concentration of plasma corticoids. The failure of pimozide to modify the GH response to L-dopa and the stimulatory GH response to clonidine suggested that GH release in the dog is regulated predominantly by noradrenergic rather than dopaminergic mechanisms. The response to emetic, but not subemetic, doses of apomorphine indicated that the stress of emesis may act as a stimulus for GH release in the conscious dog. The data from the carbidopa experiments indicated that in the conscious, as opposed to the anesthetized state, the GH response to L-dopa has a peripheral component. Carbidopa, although significantly attenuating the emesis and behavioral responses seen with L-dopa alone, did not prevent the increase in corticoid concentration which occurred in all of the animals. The inhibition of the corticoid response to L-dopa by pimozide suggested that in the conscious dog, this central stimulatory activity of L-dopa may be mediated by a dopaminergic receptor.