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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 the calcium antagonist manidipine 20 mg/day on changes in blood pressure and renal hemodynamics in response to acute stress by the mental arithmetic test (MAT) and the cold pressor test (CPT) were investigated in 14 patients with essential hypertension (median age: 50 +/- 2, WHO stage I-II). During the drug-free period, acute stress by both MAT and CPT caused an increase in the renal vascular resistance index (RVRI) [% change in RVRI, 17% for MAT (p < 0.05) and 26% for CPT (p < 0.01)] and an increase in blood pressure [% change in mean blood pressure (MBP): 17% for MAT (p < 0.001) and 16% for CPT (p < 0.001)]. CPT stress resulted in a reduction in RAFV (% change in RAFV: -12%, p < 0.05). Oral administration of manidipine resulted in hypotensive effects at rest [MBP: from 116 to 99 mmHg, p < 0.001], no change in RAFV (31.3 to 32.9 cm/sec, p = ns), and reduced RVRI (from 3.9 to 3.2 mmHg.sec/cm, p < 0.02). Manidipine inhibited the hypertensive response to acute stress by both MAT and CPT [% change in MBP: from 17% to 11% for MAT (p < 0.02) and from 16% to 11% for CPT (p < 0.01)] and also inhibited the increase in RVRI [% change in RVRI: from 17% to -1% for MAT (p < 0.05) and from 26% to 8% for CPT (p < 0.01)]. Manidipine has beneficial effects on blood pressure and renal hemodynamics at rest in patients with essential hypertension.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The effect of manidipine on renal hemodynamics in essential hypertensive patients: responses to acute stress. 134 77

Basing on the hypothesis that disturbances of cerebral information processing on the basis of acute or chronic stress situations or profound neurotic alterations are being directed to the cardiovascular system only by predisposition to hyperreactivity, the influence of a psycho-nervous-humoral-hormonal stepped load schedule upon central nervous and vegetative functions was studied in baboons. Stochastic interventions into the natural day-night rhythm and application of NaCl and DOCA doses not per se causing a blood pressure rise, either single or in combination for altogether 3 years were used as disturbing factors. It has been revealed that experimental disturbance of the light-dark phases led to lasting deviations of the conditional-reflectory activity in the sense of a predominance of irritation processes. With motor response time, initially unchanged but from the second year of experiment significantly shortened by 35%, the failure rates at differentiation increased, on the average, from 6 to 45% and the intersignal responses by 100%. Even after exposure for several months, no disorders of the cardiovascular system occurred. It was only the coupling with an experimentally induced disturbance of electrolyte distribution that provoked a significant increase in mean arterial pressure, on the average, by 24% of the pre-control value with moderate increase of the circulating blood volume. The increases in free fatty acids and blood glucose concentrations by 14 and 23%, respectively, can be interpreted as additional hypertension-favouring factors. Despite an application of mineral corticoids for more than 1 year, it has been impossible to alter the contraction behaviour of the vascular smooth muscle cell in the sense of an experimentally induced predisposition to arteriolar hyperreactivity outlasting the discontinuation of disturbing factors. With higher nervous activity being clearly disturbed as before, the pressure got back to normal; testing the vascular reactivity to noradrenaline (1.0 microgram/kg b.w/min i.v., for 5 min) or angiotensin II (0.5 microgram/kg b.w. i.v.) at the end of the investigation period gave no enhanced pressure responses. By contrast, animals exposed exclusively to the described combination load for 18 weeks, showed a still normal system pressure and sensitivity to the applied noradrenaline and angiotensin II increased by 75-120% of the pre-control response. A liability of the cardiovascular system at acute stress situations (multiple partial immobilization) in long-term neurotically predamaged monkeys in the 24-h experiment was impressive by a cardiodepression during the nightly regeneration phase, reduced on the average by 35 beats/min against the control group. Thus, our results support the hypothesis of a cerebro-visceral pathoconstellation as the etiological principle of certain forms of the inhomogeneous clinical picture of primary hypertension.
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PMID:[Arterial hypertensive dysregulations on the basis of a cerebro-visceral stimulus constellation in baboons]. 712 52

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

The diseases of chronic stress include migraine, essential hypertension, depression, and the metabolic syndrome. A theory is presented to explain how acute stress becomes chronic and causes these inter-related conditions. The theory is based on a new "circuit of emotion", which is derived from Papez' famous theory of emotion. The hypothesis is as follows: There is a basic circuit of emotion which runs from the hippocampus (defined as the dentate gyrus plus the CA regions), where emotion arises, to the amygdala and from there to serotonergic pacemaker cells in the dorsal raphe nucleus (DRN). The DRN projects back to the dentate gyrus in two ways: a direct route without a stop and an indirect route via pacemaker cells in the entorhinal cortex. The purpose of the direct route is to promote neurogenesis in the subgranular zone of the dentate; the indirect route has two purposes: to imprint ongoing moments of consciousness onto new dentate cells for retention as memory and to provide a negative feedback loop for regulation of the whole process. The hippocampus, the amygdala, and the DRN all project to the hypothalamus, which are branches off the basic loop that subserve the autonomic expression of emotion. Pathologic overdrive of the DRN causes overdrive of the entorhinal cortex, which leads to excitotoxic cell death of neurons in the hippocampus involved in the negative feedback loop. The disinhibited amygdala and DRN are then free to orchestrate the syndromes of chronic stress. Recovery from chronic stress requires repopulation of the dentate gyrus and restoration of the feedback loop. Excitotoxic cell death in the hippocampus results from either extraordinary acute stress or increased susceptibility to DRN overdrive, as might be caused, for example, by genetic factors, age, high cortisol levels, or incomplete recovery from previous damage. Three goals for therapeutic intervention are identified: inhibition of pacemaker cells in the DRN (which can be targeted by ethosuximide and other drugs that block serotonergic pacemaker currents), inhibition of pacemaker cells in the entorhinal cortex (which can be targeted by anti-epileptic drugs that block pacemaker currents in the entorhinal cortex, e.g. phenytoin), and restoration of serotonin levels in the dentate gyrus (which can be accomplished with anti-depressants). It is logical to use drugs from all three categories, either alone on in combination, to treat any of the four diseases of chronic stress. This leads to novel therapeutic recommendations, e.g. the use of ethosuximide, mood-stabilizers, and anti-depressants in synergy to treat essential hypertension.
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PMID:Redrawing Papez' circuit: a theory about how acute stress becomes chronic and causes disease. 1737 5

The expression 'hypertensive urgencies' includes many diseases. The unifying features of these diseases are a high level of arterial pressure and acute distress of one or more organs. The aim of the review was to define the idea of the 'acute hypertension' as a new concept, different from 'chronic hypertension'. Acute hypertension might be related to 'organ damage' because it is the cause, the consequence or an effect of the acute stress. We compounded a narrative review which has included analyses of 373 articles. The structure of the search strategy included a literature search of PubMed, MEDLINE, Cochrane Library and Google Scholar databases. We applied the following inclusion criteria: prospective double-blind randomised controlled trials, experimental animal work studies, case-control studies and recruiting patients representative of the general sick population. In this review, the diseases included in the term 'hypertensive emergencies' share 'acute' hypertension. This is a new idea that emphasises the suddenly increased arterial pressure, irrespective of the initial arterial pressure and independent of the goals of hypertension control. The 'hypertensive emergencies' have been grouped together in three subsets: (1) diseases that result from acute hypertension that is caused by faulty regulation of the peripheral circulation (acute primary hypertension), (2) diseases that produce hypertension (acute secondary hypertension) and 3) diseases that have hypertension as an effect of the acute stress caused by the principle disease (acute associated hypertension). This review highlights a novel idea: acute hypertension is a common sign of different diseases characterised by the sudden surge of arterial pressure, so overwhelming the difference between hypertensive emergencies and urgencies. The judgment of acute hypertension is independent of the initial arterial pressure, normotension or hypertension and is linked with the transient failure of the baroreflex. Hypertensive emergencies are grouped together because all of these diseases require prompt therapy to prevent the negative outcomes of acute hypertension.
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PMID:Hypertensive emergencies: a new clinical approach. 2689 30