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

The effects of transcendental meditation (TM) on plasma renin activity (PRA) and plasma concentrations of aldosterone, cortisol, and lactate were studied by measuring these variables before, during, and after 20--30 min of meditation. Subjects, who rested quietly rather than meditating, served as controls. There were no differences in the basal values for these variables between meditators and controls, but controls, in contrast to meditators, showed a significant increase in cortisol between the first (A) and second (B) samples of the control period. PRA increased slightly (14%) but significantly (p less than 0.03) during TM, but not during quiet rest in controls. Cortisol decreased progressively (after sample B) throughout the experiment to the same degree in both groups. Aldosterone and lactate did not change. The data do not support the hypothesis that TM induces a unique state characterized by decreased sympathetic activity or release from stress, but do suggest that meditators may be less responsive to an acute stress.
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PMID:Renin, cortisol, and aldosterone during transcendental meditation. 37 2

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

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

In a randomised controlled study in 16 orthopaedic patients, the influence of midazolam-fentanyl-N2O/O2 anesthesia (group A) resp. halothane-N2O/O2 anesthesia (group B) on the plasma concentrations of the endocrine parameters ACTH, aldosterone, cortisol, 17-DHEA, insulin, prolactin, T3, T4, TBG (thyroxine bounded globuline) as well as adrenaline, noradrenaline, and dopamine was investigated. Additionally the metabolites glucose, lactate, free glycerin, and acetacetate were measured. Beside prolactin values, only the values for ACTH, aldosterone, cortisol, and 17-DHEA differed with respect to both anesthesia methods. Under halothane-N2O/O2 anesthesia free T4 rose initially also, here represented by T4/TBG-ratio (= FTI). However, the fall of T3 concentration showed no phase - resp. anesthesia-specific changes. Catecholamine levels reached highest values towards the end of operation resp. one hour after extubation in both groups. The insulin secretion, however, was not significantly raised in either group during acute stress phases. As an expression of modified metabolic regulation comparable rises of plasma levels of glucose, lactate, free glycerin, and acetacetate were observed under midazolam-fentanyl-N2O/O2 anesthesia as well as under halothane-N2O/O2. According to presented data, both methods of anesthesia modulated the endocrine metabolic response of the organism to surgical stress, without showing any clinically relevant advantages or disadvantages attributable to either method.
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PMID:[Endocrine reaction pattern: midazolam-fentanyl anesthesia versus inhalation anesthesia]. 329 79

The effects of dietary Na+, K+, and Cl- and of acute stress on plasma levels of Na+, K+, aldosterone, and corticosterone were evaluated in vivo in birds. The dietary effects were studied in growing White Rock chicks, whereas the larger turkey was preferred for the acute stress study. Although plasma corticosterone remained unaffected, plasma aldosterone concentration decreased with increasing levels of dietary Na+ reaching a minimum at a dietary level of 72 meq/kg. Plasma Na+ remained unchanged when dietary Na+ levels increased up to 72 meq/kg but then rose with increasing Na+ intake. Plasma K+ was slightly depressed by high levels of dietary Na+ and increased by dietary K+. Neither plasma Na+ nor circulating adrenal hormones were affected by dietary K+ or dietary Cl-. Acute stress stimulated both aldosterone and corticosterone without any effect on the levels of the plasma minerals. The results suggest that of the two main corticoids, only aldosterone responds to dietary Na+ in chicks. This is in contrast to the indiscriminate stimulation of both hormones by stress, indicating different pathways of stimulation. The results also suggest that aldosterone is involved in the regulation of plasma Na+ only at low intakes of Na+ and that dietary K+ and Cl- are not involved in the aldosterone-Na+ feedback relationship.
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PMID:Concentration of adrenocortical hormones in relation to cation homeostasis in birds. 360 85

Plasma levels of corticosterone and aldosterone were determined by radioimmunoassay in ducks consuming diets containing different concentrations of sodium and potassium. Compared with control diet birds, maintenance on a high-Na+ diet for 5 days caused a 2-fold increase in the basal plasma corticosterone concentration, while adaptation for 8 days to a low-Na+ diet resulted in a 2.6-fold increase in the basal plasma concentration of aldosterone. Both corticosterone and aldosterone basal plasma levels were greatly elevated in birds denied access to drinking water for 4 days. Adaptation to a high-Na+ diet or deprivation of water resulted in hyperosmolality and hypernatremia, while the high-K+, low-Na+/low-K+, and low-Na+ diets did not significantly alter the plasma sodium or potassium levels from the control levels. In addition, birds were stressed by semi-immobilization to determine the effects of acute stress-induced ACTH secretion on the adrenocortical response following changes in dietary sodium and potassium intake. In ducks adapted to low-Na+/low-K+, high-Na+, and low-Na+ diets, stress-induced adrenocorticotrophic hormone (ACTH) increased the aldosterone, but not the corticosterone, response to a level significantly greater than in the controls. These results demonstrate that in the duck secretion of corticosterone and aldosterone can be independently regulated. Furthermore, the endocrine changes that are induced by altered sodium and potassium intake are reflected in the adrenocortical responses to acute stress.
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PMID:Effects of chronic changes in dietary electrolytes and acute stress on plasma levels of corticosterone and aldosterone in the duck (Anas platyrhynchos). 398 30

Six male subjects were acclimatized to heat; once they were given sufficient 1% saline to prevent the occurrence of a salt deficit during acclimatization, and another time they were given no saline. Plasma aldosterone (PA), plasma cortisol (PC), plasma renin activity (PRA), and plasma electrolytes were measured before, during, and after and sweat electrolytes before and after the 11-day acclimatization program. PRA and PA were significantly increased by the acute stress of heat and exercise but were unaffected by acclimatization. These increases were attenuated, but not prevented, by drinking saline, whereas sweat [Na] and PC were reduced by acclimatization but were unaffected by saline. Thus adrenocortical activity has been shown not to be increased after heat acclimatization, and mineralocorticoid activity, although potentiated by a Na deficit, appears to be determined primarily by the acute stress of heat and of exercise. Hence, the increased Na conservation with acclimatization is likely to be a normal response to heat and exercise even in the absence of a negative Na balance.
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PMID:Effect of saline loading during heat acclimatization on adrenocortical hormone levels. 626 14

The numbers and proportions of leukocytes in the blood provide an important representation of the state of activation of the immune system, and of the pattern of distribution of immune cells in the body. We have shown previously that acute stress induces large, rapid, and reversible changes in the distribution of peripheral blood leukocyte subpopulations in the rat. The studies described here specifically investigate the role played by adrenal steroid hormones in mediating stress-induced changes in blood leukocyte distribution. Since adrenal steroids act at two distinct receptor subtypes that show a heterogeneity of expression in immune cells and tissues, the role played by each subtype in mediating changes in leukocyte distribution is also investigated. Cyanoketone, a corticosterone (CORT) synthesis inhibitor, significantly reduced the decrease in lymphocyte numbers observed during stress and significantly enhanced the increase in neutrophil numbers observed after the cessation of stress. Acute administration of aldosterone (a specific type I adrenal steroid receptor agonist) to adrenalectomized animals did not have a significant effect on blood leukocyte numbers. In contrast, acute administration of CORT (the endogenous type I and type II receptor agonist), or RU28362 (a specific type II receptor agonist), to adrenalectomized animals produced changes in leukocyte distribution that were similar to those observed in intact animals during stress. These results suggest that CORT, acting at the type II adrenal steroid receptor, is a major mediator of the stress-induced changes in blood lymphocyte and monocyte distribution.
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PMID:Stress-induced changes in blood leukocyte distribution. Role of adrenal steroid hormones. 875 50

Nongenomic in vitro effects of aldosterone on the sodium-proton antiport and intracellular second messengers have been described in human mononuclear leukocytes, vascular smooth muscle cells, and endothelial cells. To test the potential physiological relevance of these effects, an in vivo 31P magnetic resonance spectroscopy study on the human calf at rest and during exercise was performed in 10 healthy volunteers receiving either 1 mg aldosterone or placebo iv in a double blind, randomized, cross-over trial. Spectra were analyzed for phosphocreatine, ATP, phosphomonoesters, inorganic intracellular phosphate, and intracellular pH. Resting values remained unchanged by aldosterone. After isometric contraction of the calf (50% body weight for 3 min), phosphocreatine recovered to significantly higher levels after application of aldosterone compared with placebo. Other parameters were not significantly changed by aldosterone. Effects appeared immediately after isometric contraction and, thus, occurred within 8 min of aldosterone administration. They are, therefore, likely to represent the first contemporary evidence of nongenomic in vivo effects of aldosterone in man. These findings also point to an involvement of aldosteron in the acute stress adaptation of cellular oxidative metabolism in human muscle physiology.
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PMID:Nongenomic effects of aldosterone on phosphocreatine levels in human calf muscle during recovery from exercise. 895 30

The classical guinea pig model for Meniere's disease, in which endolymphatic hydrops was achieved by destruction of the endolymphatic sac and obliteration of the endolymphatic duct, is a non-physiological profound model with shortcomings in relation to Meniere's disease as seen in patients. We developed a more subtle animal model; the two-phase endolymphatic hydrops. This model is based on a combination of chronic endolymphatic sac dysfunction, induced by slight destruction of the most distal part of the endolymphatic sac, and acute stress-induced endolymph production by stimulation of the Na/K-ATPase in the stria vascularis with aldosterone. Light microscopy of the fluid compartments of four groups of cochleas was used to examine them for the presence of endolymphatic hydrops: i) Normal (control) cochleas showed no hydrops; ii) some of the non-operated (no destruction) aldosterone-treated cochleas showed small degrees of hydrops mainly present in the basal turns; iii) mild dissection of the endolymphatic sac without administration of aldosterone produced a hydrops which was mainly present in the cochlear apex; iv) combination of chronic endolymphatic sac dysfunction and acute attacks of endolymph production by aldosterone administration revealed the most severe degrees of hydrops in all cochlear windings, damage to cochlear structures, and cellular disturbances of the epithelial lining of the endolymphatic sac. This new model may represent a more physiologic and dynamic approach to Meniere's disease and may explain the etiology of many symptoms in patients such as the fluctuant nature and the types of sensoneuronal hearing losses.
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PMID:Two-phase endolymphatic hydrops: a new dynamic guinea pig model. 903 74


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