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

Acute exposure of male rats to cold (5C)leads to a rapid increase of plasma levels of thyrotropin (TSH), prolactin (PRL), corticosterone, and L-thyroxine. Exposure to ether is similarly followed by a rapid increase of plasma levels of PRL and corticosterone, while TSH release is inhibited. Acute treatment with dexamethasone (500 mug) inhibits almost completely the PRL response to both exposure to cold and ether stress, while the plasma TSH response to cold is only delayed and the decrease of plasma TSH observed after ether stress is unchanged. Basal plasma levels of both TSH and PRL are lowered after treatment with the steroid. Thyroxine treatment lowers the plasma TSH concentration to undetectable levels without affecting the plasma PRL response to cold or ether exposure. The present data suggest that the rise of plasma PRL observed after cold exposure is not related to TRH and may suggest that common mechanisms control ACTH and PRL secretion during acute stress exposure.
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PMID:Effect of pharmacological blockade of ACTH and TSH secretion on the acute stimulation of prolactin release by exposure to cold and ether stress. 18 Dec 37

By means of immune fluorescence and histochemical methods, adenohypophyseal corticotropocytes from intact rats and the rats subjected to immobilization stress were studied. The data obtained demonstrated that according to their tinctorial properties, corticotropocytes are chromophobic adenocytes and some of them contain small aldehyde-fuchsinophil and PAS-positives granules. After an acute stress, corticotropocytes secrete ACTH into the intracellular space, and the cytoplasmic processes secrete it into the pericapillar space. Under a prolonged stress, the latter phenomenon prevails.
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PMID:[Immunohistochemical characteristics of cells of the adenohypophysis producing adrenocorticotropic hormone]. 19 43

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

Groups of Holtzman female rats were fed 10 mg/day of hydrocortisone succinate orally to study the responsiveness of the hypothalamic-pituitary-adrenal axis to acute stress. Pituitary ACTH content, plasma ACTH, adrenal venous corticosterone, and adrenal weights were studied simultaneously in experimental and control rats before, during, and up to two weeks after oral hydrocortisone administration. There was a significant decrease in pituitary ACTH content (p=<0.001), suppression of plasma ACTH and corticosterone in response to acute stress (p=<0.001), and adrenal atrophy during and following oral hydrocortisone administration. After discontinuing the hydrocortisone it required three to five days for the rats to respond adequately to acute stress. However, it was seven to ten days post-hydrocortisone before plasma ACTH and corticosterone responses to acute stress had returned to basal values, but decreased pituitary ACTH content and partial adrenal atrophy continued throughout the ten-day post-hydrocortisone study interval. Recovering from the suppressive effects of oral hydrocortisone was more rapid than following parenteral hydrocortisone. However, oral hydrocortisone causes identical but less sustained suppression of the hypothalamic-pituitary-adrenal axis as observed in animals treated with parenteral glucocorticoid preparations.
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PMID:Suppression of the hypothalamic-pituitary-adrenal axis after oral hydrocortisone succinate ingestion in rats. 21 74

Plasma corticosterone and plasma and pituitary ACTH concentrations were determined during feeding and after application of an acute stress at various times after food and water presentation to male rats maintained on a restricted feeding and watering schedule. Both plasma corticosterone and ACTH concentrations fell after the presentation of food and water, and this fall was accompanied by increased levels of ACTH in the pituitary gland. In addition, a rise in plasma levels of ACTH was inhibited in response to an acute stress applied at 0--5 min after presentation of food and water, but ACTH synthesis was not. This inhibition of ACTH and corticosterone secretion in response to stress was transient and dissipated as a relatively linear function of the interval between food presentation and application of the stress. The results suggest that this feeding-induced, corticosteroid-independent inhibition of pituitary-adrenal activity involves active inhibitory mechanisms operating initially on ACTH secretory processes of the pituitary and later on the synthesis of ACTH or on the secretion of hypothalamic corticotropin-releasing factor.
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PMID:Inhibition of the pituitary-adrenal response to stress during deprivation-induced feeding. 22 27

Four experiments examined the effects of stress on hypothalamic insulin and plasma hormones in rats. Two hours daily of immobilization (IM) stress for 2 and 4 days resulted in an increase in hypothalamic insulin. In contrast, 15 min of daily IM over 13 days or 48 h of continuous signalled shock avoidance did not alter hypothalamic insulin. These findings are interpreted to indicate that changes in hypothalamic insulin are part of the stress response. Possible reasons for the different effects of time and paradigm on the hypothalamic insulin responses to stress are discussed. Plasma insulin and glucose levels were not responsive to any of the stressors. Brief acute stress caused increases in the stress-responsive hormones ACTH, corticosterone, and prolactin, as expected, and these responses attenuated or disappeared with repeated or longer stress exposures.
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PMID:Effect of stress on hypothalamic insulin in rats. 132 77

Interrenal tissues from coho salmon (Oncorhynchus kisutch) were incubated in a defined medium under blood-gas atmosphere at 17 degrees. Rates of cortisol secretion by tissues incubated in media containing 50 mU/ml porcine-ACTH were initially much greater than those of resting tissues in hormone-free media, but after 3 to 6 hr returned to resting rates. The time course of cortisol accumulation in ACTH-containing media was the same when tissues were incubated in different volumes; the final concentrations of cortisol in these incubations were similar to each other and resembled peak in vivo concentrations in juvenile coho subjected to acute stress. Cortisol secretion rates of tissues sequentially transferred to fresh ACTH-containing media every 6 hr did not return to resting levels but remained elevated for at least 24 hr. Cortisol secretion in response to ACTH was attenuated or completely abolished in tissues incubated in media containing exogenous cortisol; this effect was reversible and dose-dependent. Our results suggest that in coho salmon, cortisol may exert ultra-short-loop negative feedback directly at the level of the interrenal gland to effect self-suppression.
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PMID:Evidence for ultra-short-loop feedback in ACTH-induced interrenal steroidogenesis in coho salmon: acute self-suppression of cortisol secretion in vitro. 132 52

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 dynamics of pro-opiomelanocortin (POMC) biosynthesis in the adult rat are altered by demands imposed on the system, such that acute stress increases in the efficiency of anterior pituitary (AP) posttranslational events, while repeated stress increases pretranslational events. In contrast, the developing animal has a limited adrenocortical response to acute stress during the first 2 weeks of life (stress nonresponsive period). In this study, we investigated how the maturing AP and intermediate lobe (IL) POMC cells respond to repeated demand. Measurements of AP and IL POMC mRNA and POMC peptides were performed using Northern gels and radioimmunoassay, respectively. Plasma ACTH and corticosterone measurements were also performed. Maternal isolation, for 1 h on 3 consecutive days, was used as a repeated stress stimulus. The developing AP and IL exhibit an age-related increase in POMC mRNA and peptide levels. On the other hand, AP and IL do not respond to repeated intermittent maternal isolation during the first 2 weeks of life. However, a significant corticosterone release is seen in the 14 and 21-day-old animals. A change in POMC mRNA level is only detected in the 21-day-old AP where levels decrease. Therefore, an adrenocortical response to repeated intermittent maternal isolation predates the appearance of glucocorticoid inhibition of POMC expression in the 21-day-old animal. We propose that an immature neuronal inhibitory circuit during the 3rd week of life causes a sustained corticosteroid response which may in turn trigger AP-delayed feedback.
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PMID:Development of pituitary pro-opiomelanocortin gene and peptide expression: characterization and effect of repeated intermittent maternal isolation. 143 71

We have used streptozotocin (STZ)-induced diabetes in rats to determine whether this represents a sustained stimulus to the adrenocortical system and whether STZ-diabetic rats are able to mount an acute stress response. Furthermore, we compared pituitary responsiveness to CRF and/or arginine vasopressin, and adrenal responsiveness to ACTH in STZ- vs. vehicle-treated rats. We also compared the efficacy of dexamethasone inhibitory feedback in STZ-diabetic and control rats. Our results show that STZ-treated rats chronically hypersecrete corticosterone (B) as evidenced by their decreased thymus weights, their increased urinary B excretion, and their elevated mean plasma B levels during the light hours of the day. Despite the evidence for sustained hypersecretion of B, STZ-treated rats showed greater and more prolonged ACTH and B responses to the acute stress of histamine injection. However, when tested separately, neither pituitary nor adrenal responsiveness to their secretagogues were increased in STZ-diabetic compared to control rats. Dexamethasone inhibition of stress-induced B secretion was tested using two different paradigms: pentobarbital-anesthetized rats were given iv injections of acid saline, and awake rats were given ip injections of histamine. In both experiments the STZ-treated rats were relatively resistant to glucocorticoid inhibition of stress responses. This finding, taken together with the exaggerated ACTH and B responses to stress, strongly suggests that the facilitatory effects of chronic STZ-diabetes are a consequence of changes in sensitivity of central neural components of the adrenocortical system to stimulatory and/or inhibitory inputs, in conjunction with changes in glucocorticoid feedback sensitivity.
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PMID:Chronic streptozotocin diabetes in rats facilitates the acute stress response without altering pituitary or adrenal responsiveness to secretagogues. 164 14


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