The Influence of Psychotropic Drugs and Releasing Hormones on Anterior Pituitary Hormone Secretion in Healthy Subjects and Depressed Patients

Abstract

Pharmacoendocrinological studies have shown that psychotropic drugs with different actions have different effects on anterior pituitary hormone secretion in man. Substances with different effects on the central nervous system are characterized by a different pharmacoendocrinological profile. Studies with various receptor blockers have shown varying influences on the DMI-induced growth hormone, prolactin, and ACTH/cortisol secretion. Growth hormone stimulation was shown to be mediated by alpha 2-receptors and inhibited by beta-receptors. Investigations in male and female endogenous depressive patients demonstrated a significantly blunted growth hormone response to DMI compared with age- and sex-matched healthy subjects. A comparative study in male endogenous depressive patients showed a significantly diminished growth hormone stimulation both after DMI and after growth hormone-releasing hormone compared to healthy male subjects. In further tests a simultaneous application of four releasing hormones (GHRH, CRH, GnRH, TRH) was used. These investigations showed a significantly lower GH stimulation in endogenous depressive patients compared with age- and sex-matched healthy subjects, but not in neurotic depressive or schizophrenic patients. Cortisol stimulation was similar in all groups of patients and healthy subjects. TSH stimulation was significantly lower in endogenous depressive and schizophrenic patients than in healthy subjects. Somatomedin-C concentrations were significantly elevated in endogenous depressed patients compared with healthy subjects. The blunted growth hormone response in endogenous depression could be explained by inhibitory influences such as increased somatomedin-C concentrations or a hyperactivity of central beta-adrenergic-receptors.

Comparison of the Effects of Citalopram and Escitalopram on 5-Ht-Mediated Neuroendocrine Responses

“…For example, intravenous administration of selective serotonin re-uptake inhibitors (SSRIs) produces a reliable increase in plasma prolactin as well as in plasma and salivary cortisol (Laakmann et al, 1990;Seifritz et al, 1996). The effects of acute oral administration of clinical doses of SSRIs on these neuroendocrine responses are less striking (Meltzer and Nash, 1988), but increases in plasma cortisol with citalopram (20 mg orally) and paroxetine (20-40 mg orally) have been described (Hennig and Netter, 2002;Reist et al, 1996;Kojima et al, 2003;Carpenter et al, 2003).…”

Ziprasidone decreases cortisol excretion in healthy subjects

“…Several mechanisms might be involved in the ziprasidone-mediated decrease in circulating cortisol concentrations and, therefore, in cortisol excretion. The agonist action of ziprasidone at the 5-HT1A receptor [20] and its inhibition of norepinephrine and serotonin reuptake [22] must be assumed to increase rather than to decrease HPA activity [23,26]. However, a complex interaction of the effects usually observed after reuptake inhibition and further direct effects of ziprasidone on serotonergic receptors may be important.…”

“…Acute administration of medication which potentiates serotonin or noradrenaline function stimulates the activity of the HPA axis [23]. On the other hand, blockade of 5-HT2A/C receptors antagonizes cortisol elevation in challenge experiments [24,25], whereas 5-HT1A agonism is associated with an increase in ACTH and cortisol concentrations [26].…”

Effect of Paroxetine on Thyroid Hormone Levels in Severely Depressed Patients

“…This study group therefore discussed the question as to whether SSRIs have different effects on the HPT axis than tricyclic antidepressants. It also could be demonstrated that endogenous depressive female patients showed blunted thyroid-stimulating hormone (TSH) response after releasing hormone application [7]. This did not show any effect on thyroid parameters.…”