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)

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

Recent reports suggest that centrally induced increases in sympathetic outflow to the kidney have the potential to enhance the sensitivity of pressure-dependent renin release. In the present study, the possibility was investigated that spontaneously hypertensive rats (SHR), which are thought to have increased tonic sympathetic outflow to the kidney, exhibit enhanced renin release in response to reduced renal perfusion pressure. The increase in plasma renin activity in response to a graded suprarenal aortic constriction was determined in conscious young (6-9 weeks of age) and adult (14-16 weeks of age) SHR and age-matched Wistar-Kyoto (WKY) control rats. Under conditions of relatively little stress, the renin response to reduced renal perfusion pressure was not enhanced in young or adult SHR when compared with age-matched WKY rats. That is, this regulatory mechanism was not "reset" in the hypertensive animals. When challenged with an acute stress (air to the face) both age groups of SHR exhibited a significantly enhanced response. Neither age group of WKY rats was affected by the acute air stress. These data suggest that, under unstressed conditions, pressure-dependent renin release probably does not contribute to the elevation of arterial pressure in the SHR. However, under stressful conditions, the contribution of this system may be significant. Intermittent increases in sympathetic outflow to the kidney that can occur in the SHR in response to daily stresses have the potential to render it more sensitive to spontaneous reductions in perfusion pressure. Occasional exaggerated release of renin could then contribute to the hypertensive process.
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PMID:Effect of stress on the control of renin release in spontaneously hypertensive rats. 240

In normal children aged one month to 16 years, the plasma active renin concentration (PARC) was measured with a renin immunoradiometricassay (IRMA) kit, and was compared with plasma renin activity (PRA). The IRMA for renin was found to be independent of the amount of renin substrate and not affected by the dilution of plasma samples, and was therefore proved to be a simple and reliable method. PRA measured in non-diluted plasma samples correlated well with PARC. In the age-related change, PARC in infants was significantly higher than that in older children. In infants, PARC was markedly higher in the crying state than that in the non-crying state. In normal children aged 7 to 11 years, PARC was significantly increased in the upright position compared to the supine position. These findings suggest that a hyperresponse of PARC to acute stress during blood sampling may cause an increase in active renin secretion in infants, and that stimulation by short-term standing may accelerate the activation of inactive renin or the release of active renin.
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PMID:Plasma active renin concentration in children. 268 24

The purpose of this study was to determine the influence acute stress on the plasma levels of active and inactive renin in the rat. Active and inactive plasma renins were measured in calm unanesthetized normal Wistar rats (indwelling catheter) and compared to values obtained after handling, anesthesia and decapitation. All maneuvers resulted in an increase of active renin. Only anesthesia significantly reduced inactive renin. It is concluded that acute stress can significantly change the ratio of active and inactive renins in rat plasma. These changes must be taken into consideration when the influence of "physiological or pharmacological" alterations of these enzymes are under investigation.
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PMID:The influence of acute stress on active and inactive renin in the rat. 353 27

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

A new hypothesis is presented on the function of factor XII, which is postulated to be a "missing link" between acute stress and transient hypercoagulability. The implications of this idea are developed to show how chronic stress, which involves activation of hypertension and migraine as well as hypercoagulability, can cause of cerebrovascular disease. "Acute stress" is defined as "the normal short-term physiological response to the perception of major threats or demands". "Chronic stress" is "the abnormal ongoing physiological response to the continuing perception of unresolvable major threats or demands". The factor XII hypothesis is as follows: Acute stress includes release of epinephrine by the adrenal medulla. Epinephrine activates platelets by binding to alpha-2A adrenergic receptors. Activated platelets convert pre-bound factor XII to its active form, which then initiates the intrinsic coagulation cascade. This can be called the "activated platelet initiation pathway" for coagulation. Neither tissue factor nor pre-formed thrombin is required. Thrombosis proceeds to completion, but only a minute amount of thrombin is formed, and the process normally stops at this point. In people who lapse into a state of chronic stress, essential hypertension, which is also a manifestation of stress, synergizes with hypercoagulability: there is both a baseline rise in blood pressure and systemic platelet activation as well as superimposed labile rises of both. Upregulation of these two stress parameters is atherogenic: epinephrine-activated platelets stimulating thrombin formation interact with endothelial cells activated by angiotensin II to cause, first, smooth muscle cell proliferation, which is a histological hallmark of atherosclerosis, and, lastly, a symptomatic thrombotic occlusion-the stroke. The migraine symptoms which often accompany this process are a marker of chronic stress and ongoing pathophysiologic damage. Therapeutic predictions are made regarding novel ways of blocking stress-induced hypercoagulability and hypertension. Hypercoagulability could be targeted by monoclonal antibodies directed against the platelet-specific alpha-2 adrenergic receptor or the (putative) platelet receptor for Factor XII; hypertension could be treated with monoclonal antibodies directed against the beta-adrenergic receptor in the juxtaglomerular apparatus or by surgical denervation of the kidneys, either of which would decrease the renin release which helps drive the hypertension.
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PMID:Factor XII (Hageman factor) is a missing link between stress and hypercoagulability and plays an important role in the pathophysiology of ischemic stroke. 1675 26

Critical illness induces among other events production of proinflammatory cytokines that in turn interfere with insulin signaling cascade and induce insulin resistance on a postreceptor level. Recently, local renin-angiotensin system of adipose tissue has been suggested as a possible contributor to the development of insulin resistance in patients with obesity. The aim of our study was to determine local changes of the renin-angiotensin system of subcutaneous and epicardial adipose tissue during a major cardiac surgery, which may serve as a model of an acute stress potentially affecting endocrine function of adipose tissue. Ten patients undergoing elective cardiac surgery were included into the study. Blood samples and samples of subcutaneous and epicardial adipose tissue were collected at the beginning and at the end of the surgery. Blood glucose, serum insulin and adiponectin levels were measured and mRNA for angiotensinogen, angiotensin-converting enzyme and angiotensin II type 1 receptor were determined in adipose tissue samples using RT PCR. Cardiac surgery significantly increased both insulin and blood glucose levels suggesting the development of insulin resistance, while serum adiponectin levels did not change. Expression of angiotensinogen mRNA significantly increased in epicardial adipose tissue at the end of surgery relative to baseline but remained unchanged in subcutaneous adipose tissue. Fat expression of angiotensin-converting enzyme and type 1 receptor for angiotensin II were not affected by surgery. Our study suggests that increased angiotensinogen production in epicardial adipose tissue may contribute to the development of postoperative insulin resistance.
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PMID:Increased angiotensinogen production in epicardial adipose tissue during cardiac surgery: possible role in a postoperative insulin resistance. 1805 86

The renin-angiotensin system (RAS) is classically considered to be a protective system for volume balance and is activated during states of volume depletion. Interestingly, one of the major pathways activating the system is the sympathetic nervous system, also the primary mediator of the acute stress response. When one further examines the cells mediating the immune site of the response, which is primarily an inflammatory response leading to defense at a locally injured area, these cells all express the ANG II type 1 receptor (AGTR1). Scattered throughout the literature are reports indicating that acute and chronic stress can activate renin and increase plasma levels of components of the RAS. Moreover, there are reports describing that ANG II can modulate the distribution and function of immune cells. Since the inflammatory response is also implicated to be central in the initiation and progression of vascular damage, we propose in this review that recurrent acute stress and chronic stress can induce a state with inflammation, due to ANG II-mediated activation of inflammatory cells, specifically monocytes and lymphocytes. Such a proposal would explain a lot of the observations regarding RAS components in inflammatory cells. Despite its attractiveness, substantial research in this area would be required to substantiate this hypothesis.
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PMID:Connecting chronic and recurrent stress to vascular dysfunction: no relaxed role for the renin-angiotensin system. 2098 Apr 10

Cardiovascular disorders (CVD) are associated with acute and posttraumatic stress responses, yet biological processes underlying this association are poorly understood. This study examined whether renin-angiotensin-aldosterone system activity, as indicated by a functional single nucleotide polymorphism (SNP) in the angiotensin converting enzyme (ACE) gene, is associated with both CVD and acute stress related to the September 11, 2001 (9/11) terrorist attacks. European-American respondents (N = 527) from a nationally representative longitudinal study of coping following 9/11 provided saliva for genotyping. Respondents had completed health surveys before 9/11 and annually for 3 years after, and acute stress assessments 9 to 23 days after 9/11. Respondents with rs4291 AA or TT genotypes reported high acute stress twice as often as those with the AT genotype. Individuals with the TT genotype were 43% more likely to report increased physician-diagnosed CVD over 3 years following 9/11, when the following variables were included in the model: (a) pre-9/11 CVD, mental health, and non-CVD ailments; (b) cardiac risk factors; (c) ongoing endocrine disorders; and (d) significant demographics. The ACE rs4291 TT genotype, which has been associated with HPA axis hyperactivity and higher levels of serum angiotensin converting enzyme (ACE), predicted acute stress response and reports of physician-diagnosed CVD in a national sample following collective stress. ACE gene function may be associated with both mental and physical health disorders following collective stress.
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PMID:Acute stress and cardiovascular health: is there an ACE gene connection? 2305 31


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