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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The authors' aim was to develop schemes of hypertension stage I-II treatment in subjects exposed to nervous and emotional stress at their jobs. These patients benefited from ambulatory monotherapy with obsidan or piracetam (improvement in psychic status, mental and muscular performance, in memory and attention). Reserpin worsened the patients' activity, mental performance and cognitive functions. Combination of piracetam plus reserpin promoted positive changes in psychic status, mental performance and amnestic function in stage IB-II hypertension. This combination is thought effective for inpatient treatment of hypertensive subjects exposed to psychoemotional stress.
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PMID:[The treatment with antihypertensive and nootropic preparations of hypertension patients working under neuroemotional stress]. 905 44

Under emotional stress (ES) the brain limbic-reticular structures are shown to change first. The integrative interaction of brain structures determines the secondary changes of cardiovascular functions. The effects of ES on autonomic functions are mediated primarily by chemical changes of brain limbic-reticular neurons to neurotransmitters and oligopeptides. Genetic and individual cardiovascular disorders under ES have been demonstrated. Mechanisms of sustained arterial blood hypertension under experimental ES are considered. It has been established that the resistance to ES is strongly dependent on the basic levels of oligopeptides and norepinephrine in the hypothalamus. Additional injections of oligopeptides enhance the resistance to ES.
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PMID:Effects of acute emotional stress on the brain and autonomic variables. 948 92

The wide distribution of corticotropin-releasing factor (CRF) and substance P (SP)-immunoreactive cell bodies, nerve terminals and corresponding receptors in pressor nuclei controlling emotion and stress implies that CRF and SP may play important roles in pressor responses of these nuclei; hence CRF or SP was microinjected into these nuclei respectively in Wistar male rats anesthetized with urethane to test this possibility. Microinjection of CRF into nucleus amygdaloideus centralis, nucleus paraventricularis, nucleus ventromedialis, lateral hypothalamus-perifornical region, periaqueductal gray matter, nucleus parabrachialis, locus coeruleus or rostral ventrolateral medulla respectively could evoke pressor responses (but CRF injection into nucleus dorsomedialis could not elicit significant pressor responses). Injection of substance P into all the above nuclei could also elicit hypertensive responses of different magnitudes, whereas normal saline injection into these nuclei had no effect. These results indicate that both CRF and SP in the above mentioned nuclei may play important roles in hypertension induced by prolonged emotional stress.
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PMID:Role of corticotropin-releasing factor and substance P in pressor responses of nuclei controlling emotion and stress. 962 22

Increasing of the noradrenaline synthesis with daily i.p. administration of synthetic noradrenaline precursor DL-Threo on the 21-25th day of life of the rats with inherited stress-induced arterial hypertension (ISIAH) resulted in a drop of basal and stress-induced blood pressure in adult animals with no changes in response of the hypothalamic-pituitary-adrenocortical system (HPAS). Reduction of the noradrenaline synthesis with daily i.p. administration of dopamine-hydroxylase inhibitor FLA-57 in 21-25th day old Wistar rats induced no arterial hypertension in adults but decreased their adrenocortical response to emotional stress. Noradrenaline deficit in the brain structures on the 4th week of life in rats seems to be associated with arterial hypertension only in presence of genetic defect determining this pathology. Changes in adult HPAS function due to shortage of noradrenaline in the brain in the end of the 1st month of life do not depend on hypertension.
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PMID:[Noradrenaline synthesis during the first week of life and development of inherited stress-induced arterial hypertension in rats]. 1020 64

A search for DNA markers of hereditary arterial hypertension in ISIAH rats was performed by means of contemporary molecular genetic approaches. The backcross rat population used for the analyses was derived from a cross of the Wistar x ISIAH F1 progeny with the Wistar rats. Hybridization of the HaeIII-digested DNA samples with the (CAC)5 microsatellite probe revealed cosegregation of the basal arterial pressure value with the 4.8-kb polymorphic DNA fragment. Examination of the DNA polymorphism by means of polymerase chain reaction with arbitrary primers showed an association of the 700-bp polymorphic DNA fragment with the increase of arterial blood pressure under conditions of emotional stress.
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PMID:[Analysis of polymorphic DNA markers cosegregation with arterial blood pressure in ISIAH hypertensive rats]. 1049 34

Many authors have investigated the role of psychic factors in the pathogenesis of idiopathic hypertension. Experimental studies have confirmed that the emotional stress induces a longterm blood pressure increase. Psychophysiologic investigations have revealed that patients with essential hypertension, when compared to the healthy population, are characterized by prompt reactions at the very initial stage of the disease, accompanied by an elevation of the biochemical and vegetative functional parameters, blood pressure in particular. It is in concordance with findings that hypertonics have hemodynamic reactions at rest quite similar to those found in normotonics under the emotional stress. Certain psychosocial factors cannot be identified as absolute causes of the disease. Their particular role varies from person to person. It depends on particular personality features whether any of these factors will be experienced as a stress. It has therefore been assumed that hypertension is a concomitant vegetative phenomenon, typical for people who have a permanent feeling of anger or for ambitious people who are under a permanent pressure of striving for success. Numerous psychological investigations have led to a conclusion that hypertonics have psychological troubles which cannot generally be considered as specific for hypertension. The question concerning the part played by such behaviour as the primary cause of the disease is still to be answered. Doubtlessly, such behaviour is frequent in hypertonics and it probably contributes to persistence of the disease, since they are more apt to stressogenic situations. These findings have resulted in formulating the therapeutic strategies with psychophysiologic orientation. At the physiological level, they resolve the increased excitement and lower the excessive reactivity of the vegetative nervous system, whereas on the psychological level, applying psychotherapy methods, they achieve both cognitive and behavioural changes.
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PMID:[Current psychological findings in essential hypertension]. 1051 97

Prolonged emotional stress is an important factor in the development of neurogenic hypertension, but its mechanism is still unclear. The purpose of the present study is to analyze the possible neural basis of hypertension induced by prolonged emotional stress. In the brain many nuclei are involved in emotional reaction, stress or defense response; among them the nucleus amygdaloideus centralis (AC) is the most important one which widely connects with other nuclei controlling emotion and stress, such as nucleus ventromedialis (NVM), nucleus dorsomedialis (NDM), nucleus paraventricularis (NPV) etc. These nuclei contain corticotropin releasing factor (CRF)- and substance P (SP)-immunoreactive cell bodies, nerve terminals and corresponding receptors. Our previous and present studies showed that microinjection of CRF or SP into these nuclei induced pressor responses. These data imply that excitation of the AC can activate many nuclei controlling emotion and stress via CRF and SP, and excessive activities of these nuclei may be the neural basis of hypertension induced by prolonged emotional stress. The present study revealed that (1) the AC pressor response to glutamate (Glu) could be reduced by preinjection of CRF antagonist (alpha-Helical CRF[9-41] or SP antagonist ([D-Pro(2), D-Phe(7), D-Trp(9)]-substance P) into bilateral NVM, (2) the NVM pressor response to Glu were decreased by pretreatment of the NDM with CRF- or SP-antagonist, (3) the AC-, NVM- or NDM-pressor responses were all attenuated by preinjection of CRF- or SP-antagonist into bilateral NPV or rostral ventrolateral medulla (RVL). The results indicate that excitation of the AC can indirectly activate the NPV and RVL to evoke pressor response via the NVM-NDM, CRF and SP are transmitters in each connection of this pathway; this is one component of the mechanism underlying the AC pressor response. Taken together with the findings of our previous studies, it provides neurophysiological basis for the above-mentioned implications.
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PMID:Corticotropin releasing factor and substance P mediate the nucleus amygdaloideus centralis-nucleus ventromedialis-nucleus dorsomedialis pressor system. 1052 35

The functional activity of the hypothalamo-pituitary-adrenocortical system (HPAS) during the development of rats with inherited stress-induced arterial hypertension (HSIAH rats) was compared with that in normotensive Wistar rats. In rats aged 2, 3, 4, 6, 8, 10, 12, and 18 weeks, competitive protein binding assays were used to estimate peripheral blood plasma corticosterone levels at rest and after 1 h of restricted mobility in mesh cylinders. Basal corticosterone levels and HPAS responses to stress were lower during ontogenesis in hypertensive rats than in Wistar rats of the same age. The exception was rats aged four weeks, when HSIAH rats started to develop hypertension and their HPAS was more sensitive to emotional stress than was the case in Wistar rats, this being associated with the greater reaction of the adrenals to ACTH. Decreased reactions of the HPAS to emotional stress in adult HSIAH rats is not associated with loss of adrenal ACTH sensitivity.
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PMID:Function of the hypothalamo-pituitary-adrenocortical system during ontogenesis in rats with inherited stress-induced arterial hypertension. 1183 56

There is an emotional pressor circuit composed of nuclei controlling emotion and stress, which may be the neurophysiological basis for prolonged emotional stress inducing hypertension. The central amygdaloid nucleus (AC) is the most important in this circuit, which widely connects with the other nuclei via its CRF (corticotropin releasing factor)-ergic and SP (substance P)-ergic projection fibers. There is another pressor system composed of the lateral septum (SL), habenula (HB), locus coeruleus (LC), and rostral ventrolateral medulla (RVL); muscarinic receptors are involved in each connection of this system. In view of the facts that the SL also plays an important role in integration of emotion and autonomic reaction, and the AC projects to the SL, it is likely that the SL-acetylcholine (ACh) pressor system is involved in the AC-emotional circuit. The present study demonstrates that injection of receptor blocker into each nucleus in the SL-ACh pressor pathway can reverse the AC pressor response, proving that the SL-HB (and HB-posterior hypothalamus)-LC-RVL pressor system is a component of the AC-emotional pressor circuit.
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PMID:Involvement of rat lateral septum-acetylcholine pressor system in central amygdaloid nucleus-emotional pressor circuit. 1191 90

The body's vasculature plays a critical role in the development of functional and structural alterations responsible for tissue and organ damage in laboratory animals and human subjects during illness and senescence, and in response to stress. Components of the vasculature, namely, major arteries such as the aorta, smaller arteries, arterioles, capillaries, post-capillary venules, and collecting central veins, all serve as conduits through which vital substrates are delivered to cellular masses and/or waste products are removed. A number of physical and neurohumoral agents known to be responsive to stress stimuli exert functional control over the vasculature. Both physical and emotional stress have been found to cause significant hemodynamic alterations. Large artery rigidity, for instance, develops rapidly following stress-induced activation of the autonomic nervous system. Associated with this process is increased release into the circulation of catecholamines and angiotensin-II. At the same time, insulin resistance develops, accompanied by nitric oxide release and changes in the immune system. The response of large arterial conduits to stress is characterized by increased pulse pressure, which in turn affects the endothelium of the arterial vessels responsible for determining total peripheral resistance. Microcirculation networks, where a large fraction of the blood volume is contained, are affected as well, and the blood in them is subject to redistribution into adjacent interstitial fluid compartments. Changes in endothelial permeability, secondary to variations in pulse pressure, can lead to interstitial edema and changes in the physicochemical properties of interstitial compartments. These changes give rise to alterations in the traffic of substrates and waste products between blood and cells. This sequence of events also takes place in the vasa vasorum microcirculation that nourishes large arteries, and likely contributes to remodeling of the vascular wall and to atherogenesis. The contribution of large artery rigidity to the morbidity and mortality associated with arterial hypertension, diabetes mellitus, heart failure, and terminal uremia, is relatively well established in human populations. In addition, it appears that aortic rigidity precedes the development of arterial hypertension in the spontaneously hypertensive rat (SHR) model, as well as in individuals with borderline hypertension. The fact that some of the functional and structural vascular alterations produced by stress are reversible reinforces the importance of developing behavioral techniques and pharmacologic agents that can successfully interrupt this pathological sequence of events.
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PMID:Vascular response to stress in health and disease. 1204 May 37


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