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Query: UMLS:C0848237 (acute stress)
4,619 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The responses of the hypothalamic-pituitary-adrenal axis during chronic stress are characterized by normal or slightly elevated plasma ACTH, increased hypothalamic corticotropin-releasing hormone (CRH) and vasopressin secretion, decreased pituitary CRH receptors and hypersensitivity of the ACTH and glucocorticoid responses to a novel stress. To determine the role of CRH and vasopressin in the pituitary hyperresponsiveness to a superimposed stress, pituitary CRH receptors and plasma ACTH responses were measured in rats receiving minipump infusions of CRH or a combination of CRH and vasopressin (VP), 50 ng/min of each for 50 h. Rats were killed by decapitation with or without exposure to ether vapor for 5 min or immobilization for 15 or 30 min, and blood was collected for ACTH and corticosterone determinations. The pituitary CRH receptor concentration measured by binding 125I-Tyr-oCRH, was reduced by 45 and 80% in CRH- and CRH-plus-VP-infused rats, respectively, with no changes in receptor affinity. Acute stress by ether exposure or immobilization had no effect on pituitary CRH receptors. Adrenal weight was significantly increased, and thymus weight decreased in CRH-infused animals, indicating activation of the pituitary adrenal axis. However, in contrast to the responses following chronic stress, the increases in plasma ACTH in response to an injection of 10 micrograms/kg CRH or acute stress were significantly lower in CRH- and CRH-plus-VP-infused rats. Furthermore the content and release of ACTH from quartered pituitaries were also decreased in chronically treated rats.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Desensitization of the hypothalamic-pituitary-adrenal axis following prolonged administration of corticotropin-releasing hormone or vasopressin. 133 16

The effect of hypoglycemic stress on the changes in water and electrolyte metabolism induced by head-down tilting (HDT) was studied. Six healthy men were subjected to postural changes (30 min standing, 2 h HDT, 1 h standing), with or without the intravenous administration of insulin at the beginning of HDT. When insulin was not given, antidiuretic hormone (ADH), cortisol, plasma renin activity (PRA), aldosterone, and catecholamine levels were decreased and atrial natriuretic polypeptide (ANP) levels increased during HDT. These changes were associated with 2.5- and 1.5-fold increases in urine flow and sodium excretion, respectively, when compared with the amounts before HDT. On the other hand, insulin-induced hypoglycemia during HDT produced increases in ADH, cortisol, PRA, aldosterone, and catecholamine levels. At the same time, an exaggerated ANP response by HDT was observed. These hormonal changes were associated with an abolishment of the increases in urine flow and sodium excretion. It is suggested that acute stress modifies the changes in fluid and electrolyte metabolism induced by HDT.
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PMID:Modification of water and electrolyte metabolism during head-down tilting by hypoglycemia in men. 147 52

Electrolytic lesion of the paraventricular nucleus (PVN) of the hypothalamus blocks the tachycardia response to stress. The current study examined the effects of chemical lesion of PVN parvocellular neurons on the cardiovascular and endocrine responses to stress and on the content of hypothalamic oxytocin (OT) mRNA levels. Acute footshock stress increased heart rate in both ibotenic acid lesion and control groups of animals; however, the tachycardia was significantly lower in animals with a PVN lesion than the controls. Lesion of the PVN also attenuated the increase in plasma OT induced by stress, 4-fold in the lesion group versus 20-fold for the controls. There was not a generalized decrease in hormonal responsiveness since the OT response to an osmotic challenge was exaggerated in the lesion group. There was no difference between the groups in the arterial pressure and vasopressin responses to acute stress. Neurotoxin lesions of the PVN also resulted in significant depletions of VP and OT in all levels of the spinal cord and decreased OT levels in the dorsal brainstem. Ibotenic acid lesions of the PVN resulted in no significant changes in OT mRNA in the PVN, SON and PP. In addition, the 48-h dehydration resulted in a significant increase in plasma OT and OT mRNA in the PVN. These data indicate that the parvocellular neurons of the PVN play a role in integration of cardiovascular and endocrine responses to both stressful and osmotic stimuli and provide further evidence that parvocellular OT and VP neurons project to the brainstem and spinal cord.
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PMID:Excitotoxin paraventricular nucleus lesions: stress and endocrine reactivity and oxytocin mRNA levels. 147 37

The relationships between stress and hypertension have been evaluated extensively. Acutely, stress has been shown to increase blood pressure by increasing cardiac output and the heart rate without affecting total peripheral resistance. Acute stress has been found to increase levels of catecholamines, cortisol, vasopressin, endorphins and aldosterone, which may in part explain the increase in blood pressure. However, a primary role for the activation of the sympathetic nervous system has recently been suggested in several studies. Studies in the rat are beginning to determine specific central nervous system pathways which transform stressful stimuli into signals triggering a cardiovascular response without direct cortical participation. Furthermore, acute stress reduces renal sodium excretion, which contributes to an increase in blood pressure. Several studies suggest that prolonged stress may predispose people and animals to prolonged hypertension and certain populations are at risk for the development of stress-induced hypertension. It is likely that prolonged stress-induced hypertension is the result of neurohormonal trophic factors which cause vascular hypertrophy or atherosclerosis. Because stress can affect measurement of blood pressure due to the phenomenon of 'white-coat hypertension', ambulatory blood pressure monitoring is emerging as an important feature in the evaluation of patients with hypertension. Finally, relaxation techniques are being used increasingly in the treatment of patients with hypertension.
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PMID:Stress and hypertension. 225 76

Hormones of the limbic-hypothalamic-pituitary-adrenocortical (LHPA) system are much involved in central nervous system regulation. The major LHPA neuropeptides, corticotropin-releasing hormone (CRH), vasopressin (AVP) and corticotropin (ACTH) do not only coordinate the neuroendocrine response to stress, but also induce behavioral adaptation. Transcription and post-translational processing of these neuropeptides is regulated by corticosteroids secreted from the adrenal cortex after stimulation by ACTH and other proopiomelanocortin derived peptides. These steroids play a key role as regulators of cell development, homeostatic maintenance and adaptation to environmental challenges. They execute vitally important actions through genomic effects resulting in altered gene expression and nongenomic effects leading to altered neuronal excitability. Since excessive secretory activity of this particular neuroendocrine system is part of an acute stress response or depressive symptom pattern, there is good reason to suspect that central actions of these steroids and peptides are involved in pathophysiology determining the clinical phenotype, drug response and relapse liability. This overview summarizes the clinical neuroendocrine investigations of the author and his collaborators, while they worked at the Department of Psychiatry in Mainz. The major conclusions from this work were: (1) aberrant hormonal responses to challenges with dexamethasone, ACTH or CRH are reflecting altered brain physiology in affective illness and related disorders; (2) hormones of the LHPA axis influence also nonendocrine behavioral systems such as sleep EEG; (3) physiologically significant interactions exist between LHPA hormones, the thyroid, growth hormone, gonadal and other neuroendocrine systems; (4) hormones of the LHPA axis constitute a bidirectional link between immunoregulation and brain activity; and (5) future psychiatric research topics such as molecular genetics of affective disorders, familial risk studies, drug response analysis and neurobiology of aging will benefit from extended knowledge of neural corticosteroid effects at a clinical, cellular, and molecular level.
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PMID:Psychiatric implications of altered limbic-hypothalamic-pituitary-adrenocortical activity. 267 May 76

The role of central nervous system arginine vasopressin (AVP) and oxytocin (OXY) in the cardiovascular response to acute stress was examined using three experimental models: pharmacological antagonism of central AVP-OXY receptors; lesions of the paraventricular nucleus (PVN); and rats genetically lacking in AVP synthesis, i.e., the Brattleboro strain. Central administration of an AVP-OXY antagonist abolished the increase in heart rate (HR) seen following acute footshock stress. The group receiving centrally administered antagonist increased HR 15 +/- 17 (SE) beats/min, whereas, in contrast, the group receiving intravenous administration of the antagonist showed a 66 +/- 17 beats/min increase, and the group receiving intraventricular antagonist vehicle showed a 101 +/- 14 beats/min increase in response to stress. In a second study, electrolytic lesions of the PVN also blocked the increase in HR seen following stress, 20 +/- 12 beats/min for PVN-lesioned rats, 74 +/- 25 beats/min for sham lesion rats, and 93 +/- 7 beats/min for rats with a lesion not destroying the PVN. In the final study, the responses of Brattleboro rats, i.e., rats genetically deficient in vasopressin synthesis, were equivalent to their Long-Evans controls (131 +/- 13 and 147 +/- 12 beats/min, respectively). In each of these studies, the blood pressure responses to the stressor were equivalent for control and experimental groups. The results of these studies suggest that a neuropeptide system originating in or passing through the PVN may play an important role in the cardiovascular responses to stress and further suggest that the central OXY system may be one pathway mediating this response.
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PMID:Central oxytocin systems may mediate a cardiovascular response to acute stress in rats. 271 34

The plasma oxytocin (OT) response to acute stress was compared between virgin, lactating, and hyperprolactinaemic female rats. In virgin rats, brief immobilization was associated with a significant elevation of plasma OT to 24.7 +/- 3.7 pmol/l compared with 7.7 +/- 1.1 pmol/l in controls. In contrast, the stress response was absent in lactating (6 days post-partum) animals: control OT 9.4 +/- 2.2, immobilized OT 9.0 +/- 1.1 pmol/l. Hyperprolactinaemia produced by treatment with either dopamine antagonists (domperidone or haloperidol) or ovine prolactin was also associated with an impairment of the OT stress response in intact females, whereas domperidone treatment failed to modify the response in ovariectomized (OVX) rats. Following ovarian steroid replacement with oestradiol and progesterone, the inhibitory effect of domperidone was observed in OVX rats: control OT 11.1 +/- 2.5, immobilized OT 16.0 +/- 3.7 pmol/l. Treatment of OVX rats with oestradiol and progesterone, either separately or combined, did not modify the OT stress response. Plasma levels of vasopressin were not significantly modified in either control or immobilized rats of any experimental groups. The results indicate that hyperprolactinaemia may be a causative factor in the impairment of OT stress responses observed in lactating rats.
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PMID:Oxytocin responses to stress in lactating and hyperprolactinaemic rats. 369 84

The effect of stress on drinking, water balance and endocrine profile was studied using ten castrated rams. Individual sheep were exposed to 30-h periods of total isolation (psychological stress) or physical separation from their social group (control). Plasma was analysed for haematocrit, osmolality, electrolyte levels and concentrations of cortisol and arginine vasopressin. Isolation stress significantly reduced water intake, increased haematocrit and plasma concentration of cortisol, but did not alter osmolality or vasopressin concentration. The physiological effects of this self-imposed water restriction contrast with those obtained by depriving the sheep of water for 24 h under conditions that were not stressful, i.e. by keeping them grouped together. These results suggest that cortisol may act to defend plasma volume in sheep exposed to acute stress. The results also indicate that vasopressin probably should not be considered to be a 'stress hormone' in the sheep.
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PMID:Endocrine and behavioural factors affecting water balance in sheep subjected to isolation stress. 381 41

Somatostatin (SRIF) and vasopressin (AVP) were measured in hypothalamic and extrahypothalamic areas in normotensive Wistar-Kyoto (WK) and in spontaneously hypertensive, adult rats (SRH) under control conditions and after acute immobilization stress. Hypothalamic areas included the median eminence (ME) and the periventricular, suprachiasmatic, paraventricular, supraoptic, ventromedial and dorsomedial nuclei. Extra-hypothalamic areas included the striae medullaris, striae terminalis (N. Interst.), locus coeruleus, central gray, Areas 1 and 2 (NTS), and circumventricular organs. Under basal conditions, SHR and WK rats did not differ in their content of SRIF and AVP for most areas examined. After acute stress, however, striking differences were found in peptide content. Somatostatin content was not changed in SHR, but was significantly decreased in most areas in WK rats. On the contrary, generalized increases in AVP content were found in SHR after stress, with no changes in WK animals. An exception was the ME, which showed a decrease in peptide levels in both groups of rats. These results suggest that both hypothalamic and extra-hypothalamic AVP and SRIF are involved in the central stress response. The different changes in peptide levels observed for SHR and normotensive rats after acute stress further support the hypothesis of a role of both AVP and SRIF in central regulation of cardiovascular function.
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PMID:Changes in brain somatostatin and vasopressin levels after stress in spontaneously hypertensive and Wistar-Kyoto rats. 610 6

Hyponatraemia and hypoosmolality in patients with central nervous system (CNS) disease or trauma are often ascribed to inappropriate secretion of antidiuretic hormone. A "cerebral" aetiology has been postulated. A review of published reports and data from the present study indicate that the increase in antidiuretic activity in these conditions is generally to be expected and is therefore appropriate. It is suggested that the hyponatraemia observed is the result of excessive administration of fluids. In patients with CNS disease or injured brains intravenous fluid intake should be limited to about 1 litre (of 2.5% glucose in 0.45% saline for a 70 kg adult) per day during the acute stress.
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PMID:Is "cerebral hyponatraemia" iatrogenic? 612 62


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