atrial-natriuretic-factor and Depressive-Disorder

An escape from the dexamethasone-induced suppression of pituitary-adrenocortical activity can be provoked by corticotropin-releasing hormone (CRH) in depressed patients, but not in healthy controls. One important antagonist of the CRH-stimulated secretion of corticotropin (ACTH) and cortisol is atrial natriuretic hormone (ANH).. To study a potential role of ANH in the dexamethasone-CRH test, we investigated 7 healthy men who did not suppress cortisol below 40 ng/mL after they had received 0.5 mg dexamethasone the evening before.. We found 1) that the CRH-stimulated ACTH and cortisol secretion was significantly reduced by the administration of ANH in comparison to saline; and 2) that there was an increased pituitary-adrenocortical ratio.. Our results support the view that ANH may also be involved in the frequently observed nonsuppression after dexamethasone during depression. Biol Psychiatry.

Topics: Adrenocorticotropic Hormone; Adult; Atrial Natriuretic Factor; Blood Pressure; Corticotropin-Releasing Hormone; Depressive Disorder; Dexamethasone; Endocrine Glands; Glucocorticoids; Heart Rate; Hemodynamics; Humans; Hydrocortisone; Male

Clinical and preclinical studies have gathered substantial evidence that stress response alterations play a major role in the development of major depression, panic disorder, and post-traumatic stress disorder. The stress response, the hypothalamic pituitary adrenocortical (HPA) system and its modulation by corticotropin-releasing hormones (CRH),corticosteroids,and their receptors, and the roles of natriuretic peptides and neuroactive steroids are described. We review the role of the HPA system in major depression, panic disorder, and post-traumatic stress disorder and its possible relevance for treatment. Impaired glucocorticoid receptor function in major depression is associated with an excessive release of neurohormones such as CRH, to which a number of signs and symptoms characteristic of depression can be ascribed. In panic disorder, a role of central CRH in panic attacks has been suggested. Atrial natriuretic peptide (ANP) is causally involved in sodium lactate-induced panic attacks. Furthermore, preclinical and clinical data on its anxiolytic activity suggest that nonpeptidergic ANP receptor ligands may be potentially useful in the treatment of anxiety disorders. Post-traumatic stress disorder is characterized by a peripheral hyporesponsive HPA system and elevated CRH concentrations in the CSF. This dissociation is probably related to an increased risk of this disorder. We further review recent data that describe an important role of GABA(A)-receptor modulatory,3 alpha-reduced neuroactive steroids in major depression, anxiety, and its treatment. Antidepressants are effective in both depression and anxiety disorders and have major effects on the HPA system,especially on glucocorticoid and mineralocorticoid receptors. Normalization of HPA system abnormalities is a strong predictor of the clinical course, at least in major depression and panic disorder. Currently,CRH-R1 or glucocorticoid receptor antagonists and ANP receptor agonists are being studied and may provide future treatment options more closely related to the pathophysiology of these disorders.

Topics: Animals; Anti-Anxiety Agents; Antidepressive Agents; Arousal; Atrial Natriuretic Factor; Corticotropin-Releasing Hormone; Depressive Disorder; Humans; Hypothalamo-Hypophyseal System; Neurotransmitter Agents; Panic Disorder; Pituitary-Adrenal System; Receptors, Atrial Natriuretic Factor; Receptors, Corticotropin-Releasing Hormone; Stress Disorders, Post-Traumatic

Topics: Aged; Atrial Natriuretic Factor; Depressive Disorder; Electroconvulsive Therapy; Humans; Hyponatremia; Inappropriate ADH Syndrome; Male

Topics: Animals; Antidepressive Agents; Anxiety; Asthenia; Atrial Natriuretic Factor; Biomedical Research; Depression; Depressive Disorder; Drug Therapy; Epilepsy; Guinea Pigs; Haplorhini; Indoleacetic Acids; Mice; Movement Disorders; Neurocirculatory Asthenia; Neurotic Disorders; Pharmacology; Toxicology