Abstract
The two neurotransmitters noradrenaline (NA) and acetylcholine (ACh), both important modulators of GH secretion, have been hypothesised to be reciprocally dysfunctional in depressive illness. This study tested the Adrenergic/Cholinergic Imbalance Hypothesis by comparing GH responses to (a) the cholinesterase inhibitor pyridostigmine and (b) the indirect noradrenergic agonist desipramine in a depressed group (n = 9) and a matched control group. The depressed patients fulfilled criteria for DSM‐111‐R diagnosis of Major Depression: Melancholic Subtype. Three GH challenge tests were administered in each subject: desipramine, pyridostigmine and GH‐releasing hormone (GHRH). The latter was performed to determine pituitary reserve. Each subject also had a dexamethasone suppression test. GH responses (as measured by peak minus baseline values) to GHRH were significantly blunted in the depressed (26·1 ± 4·9 mU/L) compared to the control group (48·4 ± 4·9 m U/L: t = 2·2, df = 16, p < 0·05); and were positively correlated to desipramine/GH responses in both the depressed and control groups (p < 0·001). Peak GH responses to pyridostigmine were relatively increased in the depressed sample (12·2 ± 1·8 m U/L Vs 6·9 ± 1·5 m U/L; t 2·5, df = 16, p < 0·05). Within the depressed group, dexamethasone non‐suppressors had blunted GH responses to desipramine compared to those who cortisol suppressed (p < 0·05). These findings (a) lend some support to the ‘Cholinergic/Adrenergic Imbalance Hypothesis’, (b) suggest that desipramine may bring about the release of GH via the GHRH pathway and (c) blunting of the desipramine/GH response is associated with hypercortisolaemia.