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

The borderline hypertensive rat (BHR) develops severe hypertension when chronically subjected to either a high salt diet or behavioral stress. Previous research has shown that daily exercise can attenuate the development of stress-induced hypertension in the BHR. The current study sought to determine whether exercise might also exert a similar protective effect on salt-induced hypertension. Two groups of BHR were placed on a high salt diet for 20 weeks; one of the groups also engaged in daily swim training for the entire 20 week period. A third group of BHR served as maturation controls. At the end of the experimental period, direct measurement of heart rate in conscious subjects revealed a significant resting bradycardia in the trained group on a high salt diet but no significant group differences with respect to blood pressure level. Cardiovascular responses to an episode of acute stress revealed that BHR are capable of elevating pressure in response to a novel stressor after swim training. These observations suggest that exercise may be an environmental intervention capable of increasing cardiovascular responses to acute stressors.
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PMID:The effects of exercise training on salt-induced hypertension in the borderline hypertensive rat. 177 19

The present experiments were designed to test the hypothesis that adrenal epinephrine contributes to the development of hypertension in the Dahl salt-sensitive (DS) rat. All studies were carried out in conscious male DS and Dahl salt-resistant (DR) rats weighing 200-240 g. An indwelling femoral arterial catheter was placed for blood sampling and measurement of blood pressure. After 5 days of either a high salt (7% NaCI) or a normal salt (1% NaCl) dietary regimen, DS and DR rats were subjected to an acute stress paradigm (graded electrical footshock). There were no differences in basal plasma catecholamine concentrations or in the acute pressor responses to graded footshock between the four substrain/diet groups. However, in both DS and DR rats, plasma epinephrine responses to acute footshock were greater on a 7% than on a 1% NaCl diet. Additional groups of DS rats were treated with an inhibitor of adrenal phenylethanolamine N-methyltransferase, SK&F 29,661 (1-2 g/kg body wt/day) or with vehicle. Three days after placement of an arterial catheter, rats were placed on a 7% NaCl diet, and blood pressure was measured daily for an additional 3 weeks. Although SK&F 29,661 treatment was effective in reducing adrenal epinephrine content and apparent release by approximately 80%, treatment did not alter the time course of salt-induced changes in blood pressure.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Role of epinephrine in the development of hypertension in Dahl salt-sensitive rats. 239 87

Sympathetic-adrenal medullary responses to acute footshock stress were assessed in inbred Dahl salt-sensitive (S/JR) and salt-resistant (R/JR) rats by measuring plasma levels of norepinephrine (NE) and epinephrine (EPI). Ten-week-old S/JR and R/JR rats were surgically prepared with indwelling tail artery catheters which permitted direct measurements of mean arterial pressure (MAP, mmHg) and heart rate (HR, beats/min) and remote sampling of blood. Two days after surgery, S/JR and R/JR rats were subjected to an acute stress paradigm. Blood samples were collected before and 3 minutes after transfer of rats to a shock chamber, after 1 minute of intermittent footshock, and again 5 minutes later. S/JR rats had significantly higher resting MAP's compared to R/JR rats. In contrast, baseline heart rates were similar for rats of the two strains. Basal plasma levels of NE and EPI were also similar in S/JR and R/JR rats. Upon transfer from the home cage to a shock chamber, S/JR rats exhibited significant increases in plasma levels of both catecholamines, while R/JR rats maintained circulating levels of NE and EPI that were near baseline values. However, S/JR and R/JR rats had similar increments in plasma NE and EPI following acute footshock stress. Five minutes after footshock, levels of NE and EPI returned toward baseline values for R/JR's, but remained significantly elevated above baseline in hypertensive S/JR rats. These data suggest that S/JR rats are more responsive than R/JR controls to the mild stress of transfer, but exhibit comparable responses to the more intense stress of inescapable footshock.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Sympathetic-adrenal medullary responses to acute stress in Dahl hypertensive (S/JR) rats. 272 39

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 SHR shows chronic elevations in blood pressure in response to stress or a high salt diet, at least in some studies. Stress and salt have also been combined in studies in the SHR. Tonic levels of blood pressure are not clearly elevated by superimposing acute stress on top of a chronic high salt diet. The BHR is a new model with lower resting blood pressure and marked sensitivity to environmental stressors such as stress and dietary salt intake. In the present study, SHR, BHR, or WKY were placed on a normal or high salt (8% in chow) diet. During the 8th week of the appropriate diet, blood pressure and heart rate were monitored during rest and footshock stress. Salt elevated the resting blood pressure in all three strains, but only marginally in the WKY. Stress did not further elevate the effect seen with salt, although it had a differential effect on heart rate in the three strains. In SHR, the salt group had a higher heart rate, although in BHR it was no different, and in WKY it was lower, than that seen in same-strain normal diet groups. The results are discussed in terms of the ability of the combination of stress and chronic high salt intake to alter baroreflex function in SHR, although only marginally affecting it in BHR. WKY, on the other hand, do not show evidence of altered baroreflex function when an acute stressor is superimposed on a high-salt diet.
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PMID:Effects of salt intake on blood pressure and heart rate responses to footshock stress in SHR, BHR, and WKY rats. 843 75

In the present study, the effect of acute and chronic immobilization stress on brain acetylcholinesterase (AChE) enzyme activity and cognitive function in mice was investigated. Mice were immobilized by strapping for 150 min. One group of mice were only immobilized once (acute stress) while in another group mice were immobilized (150 min) daily for 5 consecutive days (chronic stress). Specific AChE enzyme activity (micromol min(-1)mg(-1)) was estimated by a spectrophotometric method in the whole brain of mice subjected to acute and chronic stress. In the acute stress group, AChE activity (0.24922 +/- 0.011) in the detergent-soluble fraction was found to be significantly decreased in comparison to the control group (0.33561 +/- 0.022). Chronic stress did not cause any significant change in AChE activity in the detergent-soluble fraction. In the salt-soluble fraction, AChE activity was significantly decreased only in the chronic stress group (0.08791 +/- 0.011) as compared to the control group (0.12051 +/- 0.011). A passive avoidance test was used to assess cognitive function. The transfer latency time (TLT) from a light to dark chamber was recorded in the control and acute stress groups (30 min after immobilization is over) on day 1 (Trial I) and the following day (Trial II). The acute stress group showed an increase (178%) in TLT from Trial I to Trial II, which was significantly higher than that of the non-stress control group (75%). In the chronic stress group, Trial I was undertaken 30 min after the last immobilization, i.e. on day 5 and 24 hr later, Trial II. However, the chronically stressed mice showed an increase (70%) in TLT similar to the control group. Thus this study shows that acute immobilization stress may enhance cognitive function in mice which may be attributed to a decrease in AChE activity leading to an increase in cholinergic activity in the brain.
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PMID:Immobilization stress-induced changes in brain acetylcholinesterase activity and cognitive function in mice. 1094 25

Hypothalamic parvocellular vasopressin (VP) and corticotropin-releasing hormone (CRH) in the paraventricular nucleus (PVN) are major secretagogues of corticotropin (ACTH), and central plasticity including their alteration is closely related to hypothalamic-pituitary-adrenal (HPA) axis modulation. Chronic hyperosmotic stress caused by 2% salt loading has been known to alter VP and CRH expression. We recently reported that rehydration, a recovery stage from salt loading, induced a prolonged increase in parvocellular VP mRNA expression and suggested that rehydration can modulate HPA axis function without obvious external stress. In the present study, we examined hypothalamic VP and CRH mRNA expression and their responsiveness to acute immobilization stress in control, salt-loaded and rehydrated animals, in order to clarify the precise mechanism of HPA axis regulation during rehydration. The results were further compared with plasma corticosterone and ACTH levels. Plasma corticosterone decreased during salt loading, whereas it increased during rehydration at 1 week. Basal ACTH concentration increased in 1-week-rehydrated animals, with enhanced responsiveness to the acute immobilization stress. In the hypothalamic parvocellular PVN, basal CRH mRNA levels also decreased during salt loading and increased during rehydration. Basal VP mRNA was up-regulated during both salt loading and rehydration. VP mRNA responded to additional acute stress during salt loading and rehydration, but CRH mRNA did not. These results indicate that the HPA axis activity of parvocellular neurons is still altered at 1 week of rehydration and that VP plays a dominant role in regulating ACTH release in response to acute stress. This rehydration stage may thus be a good model for analysis of post-stress sensitization of the HPA axis.
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PMID:Hypothalamo-pituitary-adrenal axis sensitization after chronic salt loading. 1130 37

Clinical studies have documented an abrupt rise in plasma endothelin-1 (ET-1) coincident with an increase in mean arterial pressure (MAP) during the response to acute stress. We therefore examined the ET(A) and ET(B) receptor-dependent effects of ET-1 on the pressor response to acute environmental stress in ET-1-dependent hypertension. Stress was induced by administration of air jet pulses (3 min) in ET(B) receptor-deficient (ET(B) sl/sl) rats fed normal salt (NS; 0.8% NaCl), high salt (HS; 8% NaCl), and HS plus the ET(A) receptor antagonist ABT-627 (5 mg.kg(-1).day(-1)) on successive weeks. MAP was chronically monitored by telemetry. Total pressor response (area under the curve) was significantly reduced in ET(B) sl/sl rats maintained on a HS vs. NS diet [-6.8 mmHg (SD 18.7) vs. 29.3 mmHg (SD 8.1) x 3 min, P < 0.05]. Conversely, the total pressor response was augmented in both wild-type [34.2 mmHg (SD 29.2) x 3 min, P < 0.05 vs. NS] and ET(B) sl/sl rats [49.1 mmHg (SD 11.8) x 3 min, P < 0.05 vs. NS] by ABT-627. Blockade of ET(B) receptors in Sprague-Dawley rats caused an increase in basal MAP that was enhanced by HS and lowered by mixed ET(A)/ET(B) receptor antagonism; none of these treatments, however, had any effect on the pressor response. These data demonstrate that increasing endogenous ET-1 suppresses the pressor response to acute stress through ET(A) receptor activation in a genetic model of ET-1-dependent hypertension. These results are consistent with reports that ET-1 can attenuate sympathetically mediated responses.
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PMID:Endogenous endothelin attenuates the pressor response to acute environmental stress via the ETA receptor. 1556 33

Aldosterone controls sodium balance by regulating an epithelial sodium channel (ENaC)-mediated sodium transport along the aldosterone-sensitive distal nephron, which expresses both mineralocorticoid (MR) and glucocorticoid receptors (GR). Mineralocorticoid specificity is ensured by 11beta-hydroxysteroid dehydrogenase type 2, which metabolizes cortisol or corticosterone into inactive metabolites that are unable to bind MR and/or GR. The fractional occupancy of MR and GR by aldosterone mediating the sodium transport response in the aldosterone-sensitive distal nephron cannot be studied in vivo. For answering this question, a novel mouse cortical collecting duct cell line (mCCD(cl1)), which expresses significant levels of MR and GR and a robust aldosterone sodium transport response, was used. Aldosterone elicited a biphasic response: Low doses (K(1/2) = approximately 0.5 nM) induced a transient and early increase of sodium transport (peaking at 3 h), whereas high doses (K(1/2) = approximately 90 nM) entailed an approximately threefold larger, long-lasting response. At 3 h, the corticosterone dose-response curve was shifted to the right compared with that of aldosterone by more than two log concentrations, an effect that was fully reverted in the presence of the 11beta-hydroxysteroid dehydrogenase type 2 inhibitor carbenoxolone. Low doses of dexamethasone (0.1 to 1 nM) failed to induce an early response, but high doses elicited a long-lasting response (K(1/2) = approximately 8 nM), similar to that observed for high aldosterone concentrations. Equilibrium binding assays showed that both aldosterone and corticosterone bind to a high-affinity, low-capacity site, whereas dexamethasone binds to one site. Within the physiologic range of aldosterone concentrations, sodium transport is predicted to be controlled by MR occupancy during circadian cycles and by MR and GR occupancy during salt restriction or acute stress.
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PMID:Mineralocorticoid versus glucocorticoid receptor occupancy mediating aldosterone-stimulated sodium transport in a novel renal cell line. 1574 93

1. The long-term level of arterial pressure is dependent on the relationship between arterial pressure and the urinary output of salt and water, which, in turn, is affected by a number of factors, including renal sympathetic nerve activity (RSNA). In the present brief review, we consider the mechanisms within the brain that can influence RSNA, focusing particularly on hypothalamic mechanisms. 2. The paraventricular nucleus (PVN) in the hypothalamus has major direct and indirect connections with the sympathetic outflow and there is now considerable evidence that tonic activation of the PVN sympathetic pathway contributes to the sustained increased level of RSNA that occurs in conditions such as heart failure and neurogenic hypertension. The tonic activity of PVN sympathetic neurons, in turn, depends upon the balance of excitatory and inhibitory inputs. A number of neurotransmitters and neuromodulators are involved in these tonic excitatory and inhibitory effects, including glutamate, GABA, angiotensin II and nitric oxide. 3. The dorsomedial hypothalamic nucleus (DMH) also exerts a powerful influence over sympathetic activity, including RSNA, via synapses with sympathetic nuclei in the medulla and, possibly, also other brainstem regions. The DMH sympathetic pathway is an important component of the phasic sympathoexcitatory responses associated with acute stress, but there is no evidence that it is an important component of the central pathways that produce long-term changes in arterial pressure. Nevertheless, it is possible that repeated episodic activation of this pathway could lead to vascular hypertrophy and, thus, sustained changes in vascular resistance and arterial pressure. 4. Recent studies have reactivated the old debate concerning the possible role of the baroreceptor reflex in the long-term regulation of sympathetic activity. Therefore, central resetting of the baroreceptor-sympathetic reflex may be an important component of the mechanisms causing sustained changes in RSNA. However, little is known about the cellular mechanisms that could cause such resetting.
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PMID:Long-term regulation of arterial blood pressure by hypothalamic nuclei: some critical questions. 1585 52


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