deamino-arginine-vasopressin and Psychotic-Disorders

The effect of lithium on the urine concentrating response to antidiuretic hormone (ADH) and the excretion of ADH has been studied in rats and man. The maximum urine osmolarity following 18 h dehydration and Pitressin (5 u) was decreased in three out of four patients during lithium treatment compared to their response to the same test in the absence of lithium. In a fifth patient, tested only during lithium treatment, the urine remained hypotonic to plasma throughout this test. Lithium increased the excretion of ADH in non-polyuric patients from 9-22 mu/24 h in the absence of lithium to 36-202 mu/24 - during lithium treatment. In four patients with lithium-induced polyuria, a diuretic acting on the distal tubules, clorexolone, reduced the polyuria. Lithium increased urine volume and the excretion of ADH in four rats receiving lithium in their diet. The response to exogenous ADH was decreased during lithium administration.

Topics: Animals; Clinical Trials as Topic; Deamino Arginine Vasopressin; Dose-Response Relationship, Drug; Humans; Kidney Concentrating Ability; Lithium; Polyuria; Psychotic Disorders; Rats; Vasopressins

It has been argued that hyperactivity of the hypothalamic-pituitary-adrenal (HPA) axis is a major biological abnormality in patients suffering from psychiatric conditions such as major depression. Both arginine vasopressin (AVP) and corticotrophin releasing factor (CRF) are responsible for stimulating the release of adrenocorticotropic hormone (ACTH) from the anterior pituitary. CRF is thought to be the predominant secretagogue under normal conditions but AVP may play a more important role in situations of aberrant/chronic stress. Studies in patients suffering from melancholic depression indicate a hyper-responsiveness to agonism at the vasopressin receptor type 1B (V(1B)); patients display a heightened ACTH release after challenge with the mixed V(1B)/V(2) (vasopressin receptor type 2) agonist desmopressin in comparison to control subjects. A V(1B) antagonist has been developed which has significant selectivity for the human V(1B) receptor over the other members of the vasopressin receptor sub-family. The compound acts as an effective antagonist at both the human recombinant receptor (stably expressed in Chinese hamster ovary (CHO) cells) and the native rat V(1B) receptor (using isolated anterior pituitary cells), blocking the induction of luciferase and the release of ACTH, respectively. In vivo the compound can block the release of ACTH after challenge with a variety of V(1B) agonists. It can also attenuate the ACTH response to acute stressors in rats. Interestingly, this compound does not modulate the activity of the HPA axis under normal basal conditions.

Topics: Adrenocorticotropic Hormone; Animals; Antidiuretic Hormone Receptor Antagonists; Arginine Vasopressin; CHO Cells; Corticotropin-Releasing Hormone; Cricetinae; Cricetulus; Deamino Arginine Vasopressin; Depressive Disorder; Humans; Hypothalamo-Hypophyseal System; Hypothalamus; Male; Mood Disorders; Pituitary Gland, Anterior; Psychotic Disorders; Rats; Rats, Sprague-Dawley; Receptors, Vasopressin; Selective Serotonin Reuptake Inhibitors

Topics: Adult; Clozapine; Deamino Arginine Vasopressin; Enuresis; Female; Humans; Male; Mandelic Acids; Parasympatholytics; Prevalence; Psychotic Disorders; Urination Disorders

Topics: Adult; Clozapine; Deamino Arginine Vasopressin; Enuresis; Humans; Male; Psychotic Disorders