Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01185 (vasopressin)
23,126 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The possibility that emotional stress suppresses footshock-induced secretion of antidiuretic hormone (VP) was tested in rats by a classical conditioning paradigm. As a training trial, rats received a flash and a brief sound (2 kHz, 0.5 s) as conditioned stimuli (CS) followed by footshocks (FS, 5 ms pulses of 3 mA intensity, 50 Hz) for 1 s period as unconditioned stimuli. Rats were trained by 100 trials repeated at an interval of 6 s. A various length of time after the training, rats were tested by CS repeated at an interval of 15 s for the period of 120 s and FS of 60 s period, which started 60 s after the CS onset. Testing CS further augmented FS-induced increase in plasma adrenocorticotrophic hormone (ACTH) but suppressed FS-induced increase in plasma VP in a time-dependent manner. The CS also increased the degree of an inhibition of motor behavior known as "freezing" behavior. Augmentation of ACTH response and suppression of VP response to testing FS were dependent on the training shock intensity. These data are consistent with the hypothesis that VP secretion is potentiated by physical but suppressed by emotional stress.
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PMID:Suppression of vasopressin secretion by classically conditioned stimuli in rats. 359 55

1. Oxytocin and vasopressin were assayed in samples of blood collected from conscious rabbits during suckling. The milk yields were determined from the weight gain of the litters.2. With normal milk yields (35-155 g), relatively high concentrations (31-375 muu./ml.) of oxytocin were present in the blood but vasopressin was detected in only one out of eight samples. It is concluded that the release of oxytocin by the milk-ejection reflex is essential for normal milk removal in the rabbit and that this hormone is released independently of vasopressin.3. When the milk yield did not exceed 15 g, an amount which could be removed by passive withdrawal from the mammary gland, vasopressin was detected in four out of five blood samples but none contained a detectable concentration of oxytocin. This result can be explained by the intervention of emotional stress which is known to block the milk-ejection reflex but which acts as a stimulus for the release of vasopressin.4. Emotional stress could inhibit the milk-ejection reflex either centrally by blocking the release of oxytocin, or peripherally by blocking the response of the mammary gland to circulating oxytocin. The absence of the hormone in blood during ineffectual suckling suggests that the block is central.
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PMID:Blood levels of oxytocin and vasopressin during suckling in the rabbit and the problem of their independent release. 549 14

In experiments on rabbits, the action was studied of vasoactive peptides angiotensin-II, bradykinin and lysyl-vasopressin, injected into the brain ventricles, on a passive defensive reaction to electrical stimulation of the ventromedial hypothalamus. It was found that angiotensin-II and lysyl-vasopressin had a pronounced inhibitory influence, while bradykinin had a facilitatory effect on this reaction. Electrical stimulation of the ventromedial hypothalamus predominantly facilitated reactions of individual neurones of the sensorimotor cortex to angiotensin-II and bradykinin. Intraperitoneal injection of P-substance to rats in conditions of an acute conflict situation producing an emotional stress, brought about a significant diminution of sudden death incidence from cardiovascular insufficiency.
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PMID:[Vasoactive peptides in the structure of defensive motivational excitation]. 617 70

1. The forebrain is a major organizer of the complex behavioural, physiological and neuroendocrine responses to environmental challenges of a stressful nature. 2. Combined physiological and neuroanatomical studies suggest that a specific forebrain-brain stem network, composed of connections between the central nucleus of the amygdala, the paraventricular nucleus of the hypothalamus, the mesencephalic cuneiform nucleus, the parabrachial nucleus and the dorsal motor nucleus of the vagus nerve, may be important for integrating behavioural and physiological responses. 3. Based on studies using bilateral electrolytic lesions of the central nucleus of the amygdala, it has become clear that the central nucleus of the amygdala is one of the key structures involved in unconditioned responses to inescapable footshock. These responses include freezing behaviour, tachycardia and the release of adrenaline, noradrenaline, prolactin and corticosterone. However, this nucleus is involved only in the freezing behaviour and bradycardiac responses to conditioned emotional stress or to social defeat. 4. Both peptidergic (corticotropin releasing hormone and vasopressin/oxytocin) and aminergic (noradrenaline and dopamine) mechanisms in the central amygdala are involved in the regulation of integrated behavioural, physiological and neuroendocrine stress responses. This is indicated by studies with an infusion of an agonist and/or antagonist of the peptides or neurotransmitters into the central amygdala of freely moving rats. Sympathetic cardiac control is intensified by corticotropin releasing hormone and oxytocin, probably by inhibiting vagal output. In contrast, vagal activity is facilitated by vasopressin, noradrenaline and dopamine.
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PMID:Forebrain pathways and their behavioural interactions with neuroendocrine and cardiovascular function in the rat. 881 49

Transient exposure of rats to high doses of dexamethasone (DEX; 500 microg/day for 5 days) produced a host of symptoms that are indicative of hypothalamic-pituitary-adrenal (HPA) axis dysregulation, such as increased adrenocortical secretion over 24 h, blunted and prolonged secretory response to emotional stress, refractoriness of adrenocorticotropin in vitro release to stimulation with the secretagogues corticotropin-releasing hormone (CRH) and vasopressin, decreased levels of mRNA encoding type II corticosteroid receptors in the hippocampus and increased numbers of transcripts encoding CRH in the paraventricular nucleus. Daily administration of melatonin (MEL; 80 microg/kg) concomitantly with, and for 5 days after discontinuation of, glucocorticoid treatment 'normalized' most of the symptoms of impaired HPA regulation caused by the exposure to DEX. While none of the treatments used caused major shifts in circadian patterns of corticosterone secretion, MEL administration was associated with diminished overall corticosterone secretion and increased sensitivity to glucocorticoid feedback. Taken together, these findings indicate that chronic MEL treatment may protect several regulatory components of the HPA axis from glucocorticoid-induced deterioration.
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PMID:Chronic melatonin treatment counteracts glucocorticoid-induced dysregulation of the hypothalamic-pituitary-adrenal axis in the rat. 963 Apr 34

The two nonapeptides arginine vasopressin and oxytocin are not only secreted from the neurohypophysis into the general circulation but are also released intracerebrally. Our recent research has focused on the release patterns and effects of oxytocin and vasopressin in brain areas, such as the septum and hypothalamus, that are thought to be involved in the regulation of (1) behavioural responses and (2) responses of the hypothalamo-neurohypophysial system (HNS) to stressor exposure in rats. The results demonstrate that combined physical and emotional stress (induced by exposure to forced swimming) selectively triggers the release of vasopressin within all brain areas under study but not into the general circulation. Under emotional stress conditions (induced by exposure to the 'social defeat' procedure), however, oxytocin rather than vasopressin release increased within the hypothalamus and septum. Experiments aimed at revealing the neuroendocrine and behavioural relevance of the local nonapeptide release provided evidence for an involvement of vasopressin in the regulation of HNS activity (within the hypothalamus) and, moreover, in acute stress-coping strategies, anxiety-related behaviour and learning and memory processes (within the septum). The observed dissociation between central and peripheral nonapeptide release not only supports the hypothesis that plasma vasopressin and oxytocin concentrations do not necessarily reflect central release patterns but also suggests vasopressin and oxytocin neurones are able to independently release their nonapeptide from different parts of their neuronal surface (e.g. from somata/dendrites vs. axon terminals). This remarkable regulatory capacity provides the basis for an differential involvement of vasopressin, and probably also oxytocin, in the co-ordination of neuroendocrine activity, emotionality and cognition at different brain levels to ensure an appropriate behavioural response of the organism to stressful stimuli.
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PMID:Behavioural impact of intraseptally released vasopressin and oxytocin in rats. 1079 14

The release of adrenocorticotropin (ACTH) from the corticotrophs is controlled principally by vasopressin and corticotropin-releasing hormone (CRH). Oxytocin may augment the release of ACTH under certain conditions, whereas atrial natriuretic peptide acts as a corticotropin release-inhibiting factor to inhibit ACTH release by direct action on the pituitary. Glucocorticoids act on their receptors within the hypothalamus and anterior pituitary gland to suppress the release of vasopressin and CRH and the release of ACTH in response to these neuropeptides. CRH neurons in the paraventricular nucleus also project to the cerebral cortex and subcortical regions and to the locus ceruleus (LC) in the brain stem. Cortical influences via the limbic system and possibly the LC augment CRH release during emotional stress, whereas peripheral input by pain and other sensory impulses to the LC causes stimulation of the noradrenergic neurons located there that project their axons to the CRH neurons stimulating them by alpha-adrenergic receptors. A muscarinic cholinergic receptor is interposed between the alpha-receptors and nitric oxidergic interneurons which release nitric oxide that activates CRH release by activation of cyclic guanosine monophosphate, cyclooxygenase, lipoxygenase and epoxygenase. Vasopressin release during stress may be similarly mediated. Vasopressin augments the release of CRH from the hypothalamus and also augments the action of CRH on the pituitary. CRH exerts a positive ultrashort loop feedback to stimulate its own release during stress, possibly by stimulating the LC noradrenergic neurons whose axons project to the paraventricular nucleus to augment the release of CRH.
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PMID:Role of the hypothalamic pituitary adrenal axis in the control of the response to stress and infection. 1100 12

Lactation is associated with physiological and behavioral changes that optimize conditions for development of the offspring. Although neuroendocrine and emotional stress responses are blunted, the central mechanisms involved are unclear. In addition to a reduction in stimulatory noradrenergic inputs to paraventricular nucleus (PVN) neurons, we demonstrate that lactation induces: (1) unique phenotypic changes in neuropeptide expression by hypothalamic PVN neurons (reduced expression of corticotropin-releasing factor (CRF) mRNA and increased expression of vasopressin mRNA in parvocellular PVN neurons); and (2) changes in pituitary sensitivity to CRF (reduced) and vasopressin (increased) as a consequence of differential CRF/vasopressin secretion into the hypophysial portal blood. Neurons in the bed nucleus of the stria terminalis (BNST) and the central amygdala (CeA) that are implicated in the control of the hypothalamopituitary-adrenal axis also display changes in lactation: expression of CRF mRNA in the CeA is reduced, consistent with the diminished responsiveness to acoustic startle observed in nursing mothers. In contrast, expression of CRF mRNA is increased in the dorsolateral portion of the BNST, probably because of the tonic increases in endogenous glucocorticoid production during this period. Using immuno-targeted lesions of CRF or vasopressin in the PVN of virgin females, we have shown that CRF neurons of the PVN send inhibitory projections to the dorsolateral portion of the BNST and stimulatory inputs to CRF neurons in the CeA. Thus, it is possible that lactation-induced changes in the activity of parvocellular PVN neurons might also modulate the expression of neuropeptides and neurotransmitters in the BNST and the amygdala.
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PMID:Hypothalamic and limbic expression of CRF and vasopressin during lactation: implications for the control of ACTH secretion and stress hyporesponsiveness. 1158 48

Previous experiments have shown that a 10-min forced swimming session triggers the release of vasopressin from somata and dendrites, but not axon terminals, of neurons of the hypothalamic-neurohypophysial system. To further investigate regulatory mechanisms underlying this dissociated release, we forced male Wistar rats to swim in warm (20 degrees C) water and monitored release of the potentially inhibitory amino acids gamma amino butyric acid (GABA) and taurine into the hypothalamic supraoptic nucleus using microdialysis. Forced swimming caused a significant increase in the release of taurine (up to 350%; P < 0.05 vs. prestress release), but not GABA. To reveal the physiological significance of centrally released taurine, the specific taurine antagonist 6-aminomethyl-3-methyl-4H-1,2,4-benzothiadiazine-1,1-dioxide was administered into the supraoptic nucleus via retrodialysis. Administration of this antagonist caused a significant increase in the release of vasopressin within the supraoptic nucleus and into the blood both under basal conditions and during stress (up to 800%; P < 0.05 vs. basal values), without affecting hypothalamic or plasma oxytocin. Local administration of the GABA(A) receptor antagonist bicuculline, in contrast, failed to influence vasopressin secretion at either time point. In a separate series of in vivo electrophysiological experiments, administration of the same dosage of the taurine antagonist into the supraoptic nucleus via microdialysis resulted in an increased electrical activity of identified vasopressinergic, but not oxytocinergic, neurons. Taken together our data demonstrate that taurine is released within the supraoptic nucleus during physical/emotional stress. Furthermore, at the level of the supraoptic nucleus, taurine inhibits not only the electrical activity of vasopressin neurons but also acts as an inhibitor of both central and peripheral vasopressin secretion during different physiological states.
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PMID:Taurine selectively modulates the secretory activity of vasopressin neurons in conscious rats. 1168 96

Emotional stress inhibits vasopressin release from the pituitary but may facilitate its release from the dendrites in the hypothalamus. We examined effects of intermittently applied footshock upon the amount of vasopressin heteronuclear RNA in the hypothalamus. The footshock decreased plasma vasopressin concentration but increased its extracellular concentration within the supraoptic nucleus. The contents of the vasopressin heteronuclear RNA in the supraoptic nucleus were significantly decreased after the shock. These data suggest that intermittent footshock decreases not only vasopressin release from the axon terminals in the pituitary, but also vasopressin synthesis in the cell bodies in the hypothalamus while the stimulus facilitates vasopressin release from the dendrites in the hypothalamus. The data also suggest differential control of dendritic vasopressin release and synthesis in the hypothalamus.
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PMID:Intermittent footshock facilitates dendritic vasopressin release but suppresses vasopressin synthesis within the rat supraoptic nucleus. 1278 46


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