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The effects on GH secretion of reserpine, alpha-methyl-p-tyrosine (alpha-MT), p-chlorophenylalanine (PCPA), and haloperidol were studied in undisturbed, unanesthetized male rats with implanted intraaortic cannulae. The effects of the various drug treatments on motor activity and brain levels of catecholamines (CAs) and 5-hydroxytryptamine (5-HT) as well as the synthesis of the biogenic amines were also studied. Reserpine (10 mg/kg, ip) completely inhibited GH secretion for at least 15 h. Repeated injections of reserpine prolonged this inhibition. Episodic GH secretion reappeared 36 h after the last administration of reserpine, at which time the behavioral inhibition and blepharospasm induced by the drug was less pronounced than after 24 h, but brain levels of CAs and 5-HT were still markedly reduced. Administration of alpha-MT (150 mg/kg; 12, 4, and 2 h before experiments) inhibited episodic GH secretion and caused marked inhibition of motor activity and brain levels of CAs but not 5-HT. The inhibition of episodic GH secretion was more pronounced with haloperidol (0.5 mg/kg; 30 min before experiments) than with alpha-MT but was not as complete as that found 12 h after administration of reserpine. Administration of p-chlorophenylalanine (300 mg/kg; 72, 48, and 24 h before experiments) had no effect on episodic GH secretion, whereas brain levels of 5-HT and 5-HT synthesis were markedly reduced.

Administration of reserpine to rats completely abolished their secretion of growth hormone (GH). Administration of clonidine stimulated the GH secretion in reserpine-pre treated animals, whereas administration of apomorphine or 5-hydroxytryptophan was ineffective. Inhibition of the catecholamine synthesis by means of α-methyltyrosine partially suppressed the GH secretion, whereas inhibition of the synthesis of 5-hydroxytryptamine (5-HT) by means of p-chlorophenylalanine had no apparent effect. The results indicate that the reserpine-induced suppression of GH secretion in rats is mediated mainly by blockade of noradrenergic mechanisms and that the normal hormone secretion requires activation of noradrenaline (NA) receptors.