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 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

Environmental stress can cause an increase in sympathetic nerve activity both in humans and animals. While centrally acting antihypertensive drugs such as rilmenidine are known to reduce sympathetic tone, it is not clear whether they also influence the cardiovascular responses to acute stress. In the present study we examined the effects of systemic treatment with rilmenidine on the sympathetic and haemodynamic responses to air jet or noise stress. Twelve conscious rabbits previously implanted with a renal nerve recording electrode were subjected to an 8 l/min stream of air directed at their face for 10 min or exposure to 10 min of white noise (approximately 85 dB). Both air jet and noise stress elicited increases in renal sympathetic nerve activity (RSNA) which were greatest in the first minute (+55+/-9% and +40+/-6%, respectively), but which quickly reached a stable level over the subsequent 9 min (+24+/-6% and +9+/-5%, respectively). This was accompanied by a small increase in heart rate (HR) and mean arterial pressure (MAP). Intravenous rilmenidine (273 microg/kg) reduced MAP from 85+/-3 mm Hg to 68+/-2 mm Hg and HR from 203+/-10 b/min to 188+/-10 b/min and lowered basal RSNA by 54%. Rilmenidine reduced the increase in RSNA seen during the first minute of air jet stress by 35% and reduced the average increase over the next 9 min by 68%. However, rilmenidine had little effect on either the initial or stable RSNA responses to noise stress. Saline treatment did not alter the RSNA responses to either air jet or noise stress. The results show that centrally-acting antihypertensive agents not only lower basal RSNA, but can differentially influence environmentally induced sympathetic responses. In addition, the differential effect of rilmenidine on noise and air jet stress suggests that they may involve quite different central processing.
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PMID:Effect of rilmenidine on the cadiovascular responses to stress in the conscious rabbit. 985 67

This study examined whether or not acute stress is linked to increases in the neurosteroid levels, which is a well-known neurotransmitters associated with stress stimuli. The ginsenoside, Rb1, was tested in order to better understand its potential effects on altering the neurosteroid levels and ultimately attenuating stress. The optimal stressed condition was checked by measuring the 5a-dihydroprogesterone (DHP) and allopregnanolone (THP) levels in the brain after immobilization stress at various times. Based on this result, an acute stress model was set up to give 30 min of immobilization stress. The DHP and THP brain levels of the stressed mice were then investigated after administering Rb1 orally (10 mg/kg). These results were compared with the neurosteroid level in the stressed mice not given Rbl. Saline was administered orally to the nonstressed mice to check the placebo effect. Acute immobilization stress induced an increase in the THP and DHP concentration in the frontal cortex and cerebellum. When Rb1 was administered orally prior to immobilization stress, the THP level in the frontal cortex and cerebellum was significantly lower than that in the stressed animals not given Rbl. On the other hand, the DHP level was lower in the cerebellum only. This suggests that the metabolism of the brain neurosteroids is linked to psychological stress, and Rb1 attenuates the stress-induced increase in neurosteroids.
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PMID:Influence of ginsenoside Rb1 on brain neurosteroid during acute immobilization stress. 1690 76