Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0848237 (acute stress)
 4,619 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In adult male rats, injection of TRH into a lateral ventricle of the brain 5 min prior to pentobarbital (PB) administration caused a significant dose-related inhibition of prolactin (PRL) release, in doses ranging from 500 to 5 ng. Among 8 TRH analogues devoid of thyrotropin-releasing activity, 6 were found to significantly suppress PB-induced PRL secretion at an intraventricular dose level of 10 microgram, and the 3 most effective in this respect were also able to counteract growth hormone (GH) release elicited by PB. The derivative [1,3'-DCM2]TRH was still potent enough to block PB-induced PRL secretion at an intraventricular dosage of 50 ng. The peptide ACTH 4--10 was ineffective, whereas another ACTH derivative H-Met(O2)-Glu-His-Phe-D-Lys-Phe-OH (Org 2766) reduced PRL release. TRH did not affect the increase of plasma PRL induced by acute stress. alpha-Methyl-p-tyrosine (alpha-MT) failed to influence the inhibiting effect of TRH on GH secretion but significantly reduced that on PRL release. p-Chlorophenylalanine (PCPA) completely blocked the antagonistic effect of TRH on all PB-induced hormonal changes, suggesting that serotoninergic mechanisms may be involved in the extra-pituitary effect of TRH.
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PMID:Antagonism of pentobarbital-induced hormonal changes by TRH in rats. 20 Apr 40

Initial and follow-up fasting serum glucose levels following acute stroke were evaluated retrospectively in 392 selected hospitalized patients. Transitory reactive hyperglycaemia was observed in a large number of patients (28% of the total series) without a history of diabetes prior to the acute cerebrovascular event. The data from this group suggest a possible relationship between the impairment of carbohydrate metabolism and the type and location of stroke since both the frequency and severity of the hyperglycaemic response were higher in patients with haemorrhagic stroke and brainstem infarction as compared with cerebral infarction. The incidence and degree of the reactive hyperglycaemia were also related to the severity of the acute stroke. There were more comatose patients in the group showing this phenomenon. Initial serum glucose levels in the latter group were higher in unconscious patients than in alert ones. In addition, hospital mortality was significantly higher in these patients. Transitory reactive increases of serum glucose levels were also observed in the majority of patients with a history of overt diabetes prior to the acute stroke. The hyperglycaemic reaction following acute stroke may be attributed to several underlying mechanisms. These include: a non-specific reaction to acute stress and tissue injury with the associated autonomic, hormonal and metabolic alterations; uncovering of underlying latent diabetes by the acute stroke; increased secretion of growth hormone due to stroke-induced hypothalamic dysfunction; and irritation of the glucose regulatory centres in the hypothalamus and brain stem by blood-laden cerebrospinal fluid or local ischaemia.
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PMID:Reactive hyperglycaemia in patients with acute stroke. 97 11

Since it has become possible to sample hypophysial portal blood from sheep without totally compromising pituitary function, several important features of the secretion of hypothalamic hormones have been elucidated. The secretion of gonadotropin-releasing hormone (GnRH) has been detailed most thoroughly with the important observation that each pulsatile discharge of luteinizing hormone (LH) is the direct result of a large secretory episode of GnRH from the hypothalamus. There is high fidelity in the GnRH relationship in terms of frequency and amplitude. During the LH surge, additional factors such as an alteration in the degree of enzymic degradation of GnRH may be important physiological mechanisms. The secretion of factors that control the release of growth hormone (GH), prolactin and adrenocorticotropic hormone (ACTH) have also been studied. Hypothalamic factors controlling GH and ACTH release do not bear such an explicit relationship to the secretory episodes of pituitary hormone as seen with the GnRH/LH axis. The factor involved in the acute stress-induced release of prolactin has not yet been identified in sheep.
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PMID:What can we learn from sampling hypophysial portal blood? 142 30

In several diseases chronic pain is associated with long-lasting pathophysiological responses which differ strongly from those observed in acute situations. When persisting, acute pain often results in physical and psychological stress which may in turn aggravate the initial pathological state. In the present work we examined the secretory patterns of pituitary hormones related to acute stress (growth hormone (GH), prolactin (PRL) and beta-endorphin (beta-END)) in rats during the phase of Freund adjuvant-induced arthritis (AIA, a model used for chronic pain studies) when chronic pain is maximum (14 and 21 days, postinoculation (PI)). Using radio-immunoassay hormones were measured in plasma samples taken every 30 min for 7 h in free-moving rats 14 and 21 days after Freund adjuvant or vehicle injection and in control animals. The total amount of GH secretion was higher at 14 and 21 days PI in AIA rats as compared to vehicle-treated and control animals, and the pulsatility of GH secretory pattern was not modified by AIA. PRL and beta-END secretion were not significantly different in arthritic rats as compared to controls. These results show that GH, PRL and beta-END responses induced by acute stress are not observed during the AIA phase when chronic pain is maximum. Thus, in our experimental conditions, beta-END and PRL do not seem to be good plasma markers of chronic pain.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Chronic pain induces a paradoxical increase in growth hormone secretion without affecting other hormones related to acute stress in the rat. 159 79

The acute stress of handling followed by confinement for a period of 1 or 24 hr caused a typical stress response in rainbow trout (elevation of plasma ACTH and cortisol) and a significant reduction in the concentration of circulating growth hormone. The chronic stress of low oxygen levels in both crowded and uncrowded tanks of fish caused a significant elevation of circulating GH levels, an effect which was abolished by the provision of additional aeration to the rearing tanks. This chronic elevation of GH levels was closely correlated with an elevation of plasma cortisol in the same fish. These findings are discussed in relation to stress-induced growth suppression and to the links between the hypothalamic-pituitary-interrenal axis and somatotrope activity.
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PMID:Effects of acute and chronic stress on the levels of circulating growth hormone in the rainbow trout, Oncorhynchus mykiss. 165 35

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

Patterns of stress-responsiveness were studied in 19 adolescent male rhesus monkeys (Macaca mulatta) who are part of the free-ranging colony on Cayo Santiago, PR. Morphometric and blood samples were obtained as each male was captured and after holding overnight. Subject heart rate was recorded on Day 2, using surface EKG telemetry. Males showed marked individual differences in cardiac and endocrine profiles which were generally unrelated to their age, size or maternal rank. Heart rate patterns were correlated with several endocrine measures: males with low and variable heart rates showed lower cortisol, higher-prolactin and higher growth hormone levels on Day 2 relative to males with higher and less variable heart rates, and their testosterone levels increased rather than decreased. Males with low and variable heart rates appear to have an endocrine response profile that is less adversely affected by acute stress, and which may potentially give them a competitive advantage in social interactions.
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PMID:Heart rate and endocrine responses to stress in adolescent male rhesus monkeys on Cayo Santiago. 278 Sep 70

Studies were undertaken to evaluate the acute responses of hypothalamic noradrenergic and dopaminergic neurons and anterior pituitary hormones to naloxone (NAL)-precipitated morphine (MOR) withdrawal in the rat. Ovariectomized female rats were rendered MOR-dependent and injected with NAL (1 mg/kg b.w., s.c.). During precipitated MOR withdrawal, a decline in norepinephrine (NE) concentrations was preceded by an increase in the level of its metabolite normetanephrine (NME) in the medial basal hypothalamus (MBH) as well as the preoptic area-anterior hypothalamus (POA-AH). Both dopamine (DA) and its major acid metabolite, dihydroxyphenylacetic acid (DOPAC), showed increased concentrations in these two hypothalamic regions within 30 min of NAL administration. Elevated luteinizing hormone (LH) and beta-endorphin secretion was evident within 5 min of NAL injection to MOR-dependent rats, while serum prolactin (PRL) increased 15 min into MOR withdrawal. Both growth hormone (GH) and thyroid-stimulating hormone (TSH) were depressed over the course of MOR withdrawal. Although a cause and effect relationship cannot be established, during NAL-precipitated MOR withdrawal, a heightened hypothalamic monoaminergic neuronal activity is accompanied by a differential response of anterior pituitary hormones. The observed responses, which are similar to those seen during acute stress, indicate that MOR withdrawal may activate the same mechanisms which mediate the neuroendocrine response to stress.
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PMID:Changes in anterior pituitary hormone secretion and hypothalamic catecholamine metabolism during morphine withdrawal in the female rat. 405 62

Plasma somatolactin (SL) concentrations in rainbow trout were examined under various physiological and environmental conditions. Background adaptation and feeding did not affect plasma SL levels. There was no consistent change in plasma SL levels during fasting for 21 days, although increased plasma growth hormone levels and decreased condition factor, hepatosomatic index and abdominal fat, occurred. Plasma SL concentrations increased during acute stress and also during exhaustive exercise resulting from being chased in shallow water. Elevation of plasma SL was associated with those of plasma cortisol, Ca2+, phosphate, and glucose levels. On the other hand, plasma level of prolactin was not affected in the stress and exercise experiments, although plasma GH and Na+ were raised in the fish 5 min after the onset of the stress. Our results suggest the involvement of SL in calcium and phosphate metabolism, acid-base regulation, or energy mobilization in the stressed or exercised trout.
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PMID:Effects of feeding, fasting, background adaptation, acute stress, and exhaustive exercise on the plasma somatolactin concentrations in rainbow trout. 763 67

The effects of acute stress on growth hormone (GH) secretion and the mechanisms involved in its changes have been investigated in sheep. An acute isolation-restraint stress induced a rapid and significant increase in jugular GH levels in 12 out of 14 rams. GH-releasing hormone (GHRH) and somatostatin secretion during the same stress were studied in 5 animals prepared for hypophysial portal blood collection. A 3.5-fold increase in portal GHRH levels was observed concomitantly with a slight elevation in portal somatostatin. Portal corticotropin-releasing hormone (CRH) and jugular cortisol plasma levels increased during the same stress. Our data suggest that an isolation-restraint stress stimulates GH secretion in the sheep and that GHRH may be responsible for GH response.
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PMID:Acute stress stimulates secretion of GHRH and somatostatin into hypophysial portal blood of conscious sheep. 781 15


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