Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0085631 (agitation)
 12,064 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The objective of this study was to determine the effects of i.v. nicotine on plasma arginine vasopressin (AVP), plasma osmolality, and behavior in the conscious monkey. Adult, female, chronically prepared monkeys (Macaca mulatta) were studied with i.v. infusion of 5% dextrose and water in control experiments without change in parameters. Nicotine infusion (100 mug/kg/min) in 14 experiments produced a significant increase in plasma AVP from control levels of 0.6 +/- 0.5 muU/ml to end-of-infusion levels of 35 +/- 17 muU/ml (p less than 0.001). During the 15-20 min of nicotine infusion, a behavioral sequence of restlessness, yawning, retching, salivation and chewing accompanied AVP release. Plasma osmolality remained unchanged. Pretreatment of the monkeys with promethazine (Phenergan) and diphenhydramine (Benadryl) at 1-5 mg/kg reduced both the plasma AVP increase and the behavioral effects. These results provide conclusive evidence that nicotine can release large amounts of AVP in the monkey.
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PMID:Vasopressin released by nicotine in the monkey. 82 17

Effects of intracerebroventricular (third ventricle) injection of N-methyl-D-aspartate (NMDA) on arterial blood pressure, on heart rate, on arginine vasopressin (AVP) and levels of catecholamines in plasma and on the behaviour of normotensive freely-moving rats have been evaluated. N-Methyl-D-aspartate significantly (P less than 0.01) increased arterial blood pressure and levels of catecholamines and AVP in plasma. With 0.1-1.0 micrograms/rat all animals presented psychomotor agitation, stereotyped movements, hyperexcitability, exophthalmus, dyspnoea, jumping, rearing and teething. The selective antagonist for NMDA receptors, 2-APV injected in the third ventricle, significantly (P less than 0.01) antagonized the hypertension, the increase in levels of catecholamines and AVP in plasma and behavioural effects. An antagonist of alpha 1 adrenergic receptors, prazosin (i.v.), an agonist of alpha 2 adrenergic receptors, clonidine (i.c.v.) and a relatively selective antagonist of V1 subtype of receptor of AVP, CGP 25838 (i.c.v. and i.v.), 15 min before NMDA, significantly (P less than 0.01) decreased the effects induced by the injections of NMDA. On the contrary, an antagonist of opiate receptors, naloxone (i.v.), 15 min before NMDA, significantly (P less than 0.01) increased the NMDA-induced modifications. Pretreatment with the antagonists at these doses, did not significantly modify the basal values of arterial blood pressure and behaviour. Only 2-APV sometimes induced ataxia, lasting about 5 min. This study points out an increase in the central sympathetic efferent activity and in release of AVP involved in the NMDA-induced cardiovascular and behavioural effects.
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PMID:Participation of arginine vasopressin-mediated and adrenergic system-mediated mechanisms in the hypertension induced by intracerebroventricular administration of NMDA in freely moving rats. 135 1

Our goal in this study was to examine where nicotine acted on the neurohypophysial release of arginine vasopressin (AVP). In the chamber-isolated, unanesthetized cat, an IV infusion of nicotine (25--50 micrograms/kg/min for 10 min) produced a 54-fold rise in plasma AVP (65 +/- 12.5 microU/ml) and a behavioral sequence of restlessness, ear twitching, salivation, chewing and retching. Chloralose anesthesia and acute surgical preparation increased plasma AVP (9.4 +/- 3.8 microU/ml) 4-times the control level in the unanesthetized state (2.4 +/- 0.1 microU/ml). In the anesthetized cat, an IV infusion of nicotine produced a 140-fold rise in plasma AVP (802.7 +/- 289.0 microU/ml) and a biphasic response in mean arterial blood pressure (MABP) which rose to 32% above control in the first 5 min and fell to 25% below control during the last 5 min. Bilateral surgical section of the carotid sinus and vagus nerves increased plasma AVP (47.6 +/- 25.8 microU/ml) to 5-times the control level in the anesthetized state (9.4 +/- 3.8 microU/ml). In the anesthetized, baroreceptor-denervated cat, an IV infusion of nicotine produced a 3-fold rise in plasma AVP (141.5 +/- 31.3 microU/ml) and a biphasic MABP response. Hypophysectomy abolished the nicotine-induced rise in AVP but did not modify the biphasic MABP response. These data suggest that in the cat nicotine releases AVP from the neurohypophysis by multiple sites of action within the receptive fields of te carotid sinus and vagus nerves and at unknown loci within the central nervous system.
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PMID:Vasopressin release by nicotine in the cat. 724 22

The effect of an acute fall in plasma cortisol on the secretion of CRH, arginine vasopressin (AVP), and ACTH was studied using our nonsurgical technique for collecting pituitary venous (PV) blood from horses. PV blood from six mares was collected continuously and divided into 30-sec segments for 0.5 h before and during a 3-h infusion of metyrapone, an 11-beta-hydroxylase inhibitor. During treatment, plasma cortisol fell (P < 0.01) to a mean nadir of 15% of pretreatment levels, and 11-deoxy-cortisol rose (P < 0.02). Three mares became mildly agitated during treatment. Mean PV concentrations of CRH (P < 0.025), AVP (P < 0.05), and ACTH (P < 0.005) were higher during the second hour of treatment than before. For AVP (P < 0.05) and ACTH (P < 0.01), the amount secreted in peaks detected by CLUSTER analysis increased during treatment, whereas peak frequency did not. Responses, particularly in CRH and AVP, tended to be amplified during agitation. Increases in CRH, AVP, and ACTH secretion commenced when cortisol had fallen to 50-59% of the initial value (P < 0.005 for each). By contrast, the cortisol concentration at this point varied 3-fold among mares. The ratio between PV concentrations of ACTH and CRH, which was used as an index of pituitary responsiveness to endogenous CRH, also rose (P < 0.005) as cortisol fell. The increase in this ratio preceded any significant change in CRH secretion and was maintained to the end of the experiment. We suggest that the initial response to falling cortisol in the horse is at the pituitary, via increased responsiveness to CRH. If cortisol continues to fall, AVP and then CRH secretion are stimulated. However, the magnitude of the hypothalamic response to hypocortisolemia may be augmented by concurrent stress. Last, the hypothalamo-pituitary-adrenal axis of the horse appears to monitor changes in plasma cortisol and not concentrations, at least in the short term.
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PMID:The acute effect of lowering plasma cortisol on the secretion of corticotropin-releasing hormone, arginine vasopressin, and adrenocorticotropin as revealed by intensive sampling of pituitary venous blood in the normal horse. 839 77

Exposure to early life stress is a predictor of mental health disorders, and two common forms of early life stress are social conflict and impaired maternal care, which are predominant features of postpartum mood disorders. Exposure of lactating female rats to a novel male intruder involves robust social conflict and induces deficits in maternal care towards the F1 offspring. This exposure is an early life social stressor for female F1 pups that induces inefficient lactation associated with central changes in oxytocin (OXT), prolactin (PRL), and arginine vasopressin (AVP) gene expression in adult F1 females. The mothers of the rats in the current study were either allowed to raise their pups without exposure to a social stressor (control), or presented with a novel male intruder for 1h each day on lactation days 2-16 (chronic social stress). The effects of this early life chronic social stress (CSS) exposure on subsequent peripheral endocrinology, maternal behavior, and physiology were assessed. Exposure of female pups to early life CSS resulted in persistent alterations in maternal endocrinology at the end of lactation (attenuated prolactin and elevated corticosterone), depressed maternal care and aggression, increased restlessness and anxiety-related behavior, impaired lactation, and decreased saccharin preference. The endocrine and behavioral data indicate that early life CSS has long-term effects which are similar to changes seen in clinical populations of depressed mothers and provide support for the use of the chronic social stress paradigm as an ethologically relevant rodent model for maternal disorders such as postpartum depression and anxiety.
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PMID:Effects of early life social stress on endocrinology, maternal behavior, and lactation in rats. 2400 86