Desipramine and Growth Hormone Secretion

Laakmann, G.; Schön, Henrik; Wittmann, Michael

doi:10.1016/s0140-6736(81)91202-2

Cited by 20 publications

(7 citation statements)

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“…The a 2 agonist clonidine (Matussek et al 1980) or the NA-reuptake inhibitor DMI (Laakmann et al 1981) are known to acutely stimulate GHRH and GH release in man via hypothalamic a 2 receptors. The a 2 blocker yohimbine has been demonstrated to significantly reduce the DMIinduced GH stimulation by postsynaptic a 2 blockade in man (Laakmann et al 1986a).…”

Section: Growth Hormone Secretionmentioning

confidence: 99%

“…Therefore, psychotropic drugs with different effects on the central neurotransmitter system have distinct effects on the anterior pituitary hormone secretion and can be characterized by certain pharmacoendocrinological profiles (Table 1). Antidepressants which primarily act via noradrenaline (NA)-reuptake inhibition [for example, desipramine (DMI)] stimulate growth hormone (GH) secretion (Laakmann et al 1981), whereas serotonin (5-HT)-reuptake inhibiting antidepressants (for example, indalpine, clomipramine) are characterized by prolactin (PRL) stimulation (Laakmann 1988). Cortisol (COR) secretion can acutely be increased by antidepressants with both NA-or 5-HT-reuptake inhibition; the stimulatory effects of antidepressants on COR secretion are mediated via stimulation of the corticotropin (ACTH) output of the pituitary gland (Laakmann 1988).…”

Section: Introductionmentioning

confidence: 99%

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The influence of mirtazapine on anterior pituitary hormone secretion in healthy male subjects

et al. 2002

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Since the acute inhibition of COR secretion in the healthy volunteers was paralleled by a simultaneous decrease of ACTH release, central mechanisms (for example, inhibition of hypothalamic CRH output) are suggested to be responsible for the inhibitory effects of mirtazapine on COR secretion. Our results are of particular interest in the light of the hypercortisolism observed in depressed patients and new pharmacological approaches such as CRH(1) receptor antagonists.

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Section: Growth Hormone Secretionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

The influence of mirtazapine on anterior pituitary hormone secretion in healthy male subjects

et al. 2002

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“…Ob viously, some healthy probands and most non-depressive postmenopausal women as well as women during the menstruation period also have a blunted GH response to CLON (Matussek et al, 1984). The GHrespectively cortisol-stimulation tests with DMI (Laakmann, 1981), respectively methylamphetamine (Checkley and Cram mer, 1977;Checkley, 1979) point into the same direction.…”

mentioning

confidence: 94%

Biological Aspects of Depression

Matussek¹

1986

Psychopathology

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Several neuroendocrine studies with the clonidine-growth hormone stimulation test show endogenous depressive patients to have a reduced GH response as compared to neurotic depressives, schizophrenics and controls. The blunted GH response to clonidine seems to be a trait marker or vulnerability factor for mono- and bipolar endogenous depression. It could be explained by a reduced postsynaptic Α2-adrenoceptor sensitivity or of structures related to them. The sensitivity of Α2-adrenoceptors is influenced by both, the endorphinergic and cholinergic systems. First results supporting this concept are presented and discussed.

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“…Mean (* SEM) serum growth hormone (GH) concentrations in 9 depressed and healthy subjects at fixed intervals over a three hour period following administration of desipramine (1 mgkg body weight, to nearest 25 mg) at 0 min vious studies have found attenuated GH responses to GHRH in depression (Lesch et af., 1987 andPeabody et af., 1990). Differences in the A GH responses to desipramine between the two groups failed to reach statistical significance but this is probably due to a Type 2 error in view of the unanimity in other studies using this challenge (Laakmann et al, 1981;Meesters et al, 1985;Ryan et al, 1988, Dinan andBarry, 1990). The strong correlation between A GH responses to GHRH and desipramine lends further weight to the hypothesis that desipramine brings about GH secretion via GHRH (Katakami et al, 1984).…”

Section: Discussionmentioning

confidence: 89%

“…One of the most consistently replicated findings in depressive illness is of a diminished GH response to the a, agonist clonidine in depressed compared to healthy states (Checkley et al, 1981;Lesch et al, 1988;Amsterdam et a[., 1989). The tricylic reuptake inhibitor desipramine is thought to bring about GH release by stimulation of post-synaptic a2 adrenoceptors (Laakmann et al, 1986) and several groups have found that desipramine/GH responses are also blunted in depression (Laakmann et al, 1981;Meesters et al, 1985;Ryan er al., 1988;Dinan and Barry, 1990). GH responses to the indirect ACh agonist pyridostigmine, conversely, are enhanced in depressed compared to healthy groups (O'Keane et al, 1992).…”

Section: Introductionmentioning

confidence: 97%

Cholinergic and adrenergic function in depressed and healthy subjects: A neuroendocrine test battery using the growth hormone axis

O’Keane

Dinan

1994

Human Psychopharmacology

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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 Adrenergicl 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-11 l-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 f 4.9 mU/L) compared to the control group (48.4 f 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 f 1.8 m U/L Vs 6.9 f 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 01 < 0.05). These findings (a) lend some support to the 'CholinergidAdrenergic 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.

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Desipramine and Growth Hormone Secretion

Cited by 20 publications

References 3 publications

The influence of mirtazapine on anterior pituitary hormone secretion in healthy male subjects

The influence of mirtazapine on anterior pituitary hormone secretion in healthy male subjects

Biological Aspects of Depression

Cholinergic and adrenergic function in depressed and healthy subjects: A neuroendocrine test battery using the growth hormone axis

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