Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0020538 (hypertension)
 170,190 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.
 ...
PMID:The effects of exercise training on salt-induced hypertension in the borderline hypertensive rat. 177 19

Two inbred strains have been developed from a cross between SHR and WKY. WK-HTs are hypertensive but not hyperactive, and WK-HAs are hyperactive but normotensive. Together with SHR (that express both traits) and WKY (expressing neither trait) we used four strains to follow correlations of biological changes with the expression of hyperactivity or hypertension. We show that the well known sympathetic hyperreactivity of SHRs to acute stress is associated with the hyperactivity trait and not the hypertension among the four strains. Similarly, the well known ventricular hypertrophy in SHRs is more prominent among the hyperactive strains than the hypertensives. Examination of regional brain amine levels revealed an imbalance in forebrain serotonin transmission in the hyperactive strains, and no significant correlations with hypertension. On the other hand, neuropeptides in brainstem and spinal cord revealed a decrease, in hypertension, in neuropeptide Y and PNMT content of terminals of C1 fibers that innervate the spinal cord sympathetic outflow. Also, the two hypertensive strains showed increased TRH-and proctolin-like immunoreactivity in fibers that innervate the C1 cells in the rostral ventrolateral medulla. These findings illustrate the unique advantage provided by WK-HA and WK-HT strains as additional controls for SHRs in studying hypertension and hyperactivity.
 ...
PMID:Two new Wistar-Kyoto rat strains in which hypertension and hyperactivity are expressed separately. 183 60

In summary, according to the proposed model, race is viewed as a sociocultural designation that denotes differential exposure to chronic social stressors. It is proposed that black Americans are exposed to significantly more chronic social stressors than are white Americans. Many of these chronic social stressors have been associated with hypertension prevalence in epidemiological studies. Furthermore, chronic stress has been shown to augment cardiovascular reactivity to acute stress in both animals and humans, and to increase sodium retention in spontaneously hypertensive rats. Acute stress has also been demonstrated to increase sodium retention in humans. The essential element of our model is that chronic social stressors that are represented more within the black American population due to historical factors are related to an increase in sodium sensitivity and retention. This altered sodium metabolism may be further augmented by biological, behavioral, and psychological risk factors for hypertension and modulated by stress coping resources. It is hoped that this model will serve as a stimulus for further research on the biopsychosocial aspects of autonomic reactivity and hypertension in blacks.
 ...
PMID:Autonomic reactivity and hypertension in blacks: a review and proposed model. 184 32

The purpose of this study was to determine if the state of physical training influences sympathetic neural activation during acute stress in humans. We recorded muscle sympathetic nerve activity (microneurography of the peroneal nerve), arterial blood pressure, and heart rate in 12 highly trained, endurance athletes (25 +/- 1 years, mean +/- SEM) and 12 untrained subjects (27 +/- 1 years) before (supine rest control) and during: 1) lower body negative pressure at -5, -10, -15, and -20 mm Hg (orthostatic stress); 2) isometric handgrip at 30% of maximum (exercise stress); and 3) hand immersion in ice water, that is, the cold pressor test (thermal stress). Body weight was not different in the two groups, but the athletes had a lower body fat content (8.9 +/- 1.3% versus 16.1 +/- 2.0%, p less than 0.05). During supine rest, muscle sympathetic nerve burst frequency (24 +/- 3 versus 24 +/- 2 bursts/min, athletes versus untrained subjects) and burst incidence (36 +/- 3 versus 44 +/- 4 bursts/100 heart beats) and arterial blood pressure were not different in the two groups, but heart rate was lower in the athletes (54 +/- 2 versus 67 +/- 3 beats/min, p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)
Hypertension 1991 Jan
PMID:Sympathetic neural adjustments to stress in physically trained and untrained humans. 198 81

The relationships between stress and hypertension have been evaluated extensively. Acutely, stress has been shown to increase blood pressure by increasing cardiac output and the heart rate without affecting total peripheral resistance. Acute stress has been found to increase levels of catecholamines, cortisol, vasopressin, endorphins and aldosterone, which may in part explain the increase in blood pressure. However, a primary role for the activation of the sympathetic nervous system has recently been suggested in several studies. Studies in the rat are beginning to determine specific central nervous system pathways which transform stressful stimuli into signals triggering a cardiovascular response without direct cortical participation. Furthermore, acute stress reduces renal sodium excretion, which contributes to an increase in blood pressure. Several studies suggest that prolonged stress may predispose people and animals to prolonged hypertension and certain populations are at risk for the development of stress-induced hypertension. It is likely that prolonged stress-induced hypertension is the result of neurohormonal trophic factors which cause vascular hypertrophy or atherosclerosis. Because stress can affect measurement of blood pressure due to the phenomenon of 'white-coat hypertension', ambulatory blood pressure monitoring is emerging as an important feature in the evaluation of patients with hypertension. Finally, relaxation techniques are being used increasingly in the treatment of patients with hypertension.
 ...
PMID:Stress and hypertension. 225 76

The effect of maternal strain on reactivity to acute stress was studied in F1 reciprocals produced by crossing the spontaneously hypertensive rat (SHR) with its normotensive progenitor, the Wistar-Kyoto (WKY). This F1 generation, known as the borderline hypertensive rat (BHR), is genetically predisposed to develop hypertension in response to chronic stress or high dietary sodium. Reciprocals, considered to be genetically equivalent aside from sex-linked traits, differ in strain of dam during intrauterine and preweanling development. At 17 weeks of age, reciprocal F1 males did not differ in open-field behavior (squares crossed, rearings, and defecation measured over 3 days in 15-min sessions) or in home-cage measurements of mean arterial pressure (MAP) and heart rate (HR). However, different patterns of cardiovascular reactivity were displayed to transfer and footshock. While WKY-mothered rats reacted with graded pressor responses, SHR-mothered rats responded maximally to transfer, showed no additional increase to footshock, and maintained peak responding after footshock was terminated. Such reactivity differences may mediate the impact of environmental variables on the genetic disposition to hypertension.
 ...
PMID:Dam strain affects cardiovascular reactivity to acute stress in BHR. 232 28

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)
Hypertension 1990 Sep
PMID:Role of epinephrine in the development of hypertension in Dahl salt-sensitive rats. 239 87

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.
Hypertension 1990 Mar
PMID:Effect of stress on the control of renin release in spontaneously hypertensive rats. 240

In order to find out whether beta-endorphin (beta-E) is involved in the development of hypertension, we performed two series of experiments. Firstly, spontaneously hypertensive rats (SHR) and their normotensive Wistar Kyoto controls (WKY) were submitted to ether stress. Plasma concentrations of beta-endorphin-like immunoreactivity (beta-EI), adrenocorticotropin (ACTH) and alpha-melanotropin (alpha-MSH) were measured by radioimmunoassay. The basal concentration of beta-EI was similar in WKY and SHR, whereas WKY had higher levels of ACTH and lower levels of alpha-MSH than SHR. In both strains acute stress enhanced the plasma concentration of beta-EI to the same extent and with a similar time-course. The increase of plasma beta-EI coincided with a rise in ACTH but not alpha-MSH. Gel chromatography of beta-EI revealed that plasma extracts contain similar amounts of beta-lipotropin- (beta-LPH) and beta-E-sized immunoreactive components, and that acute stress elevated both forms of beta-EI. Secondly, isolated tail arteries of SHR and WKY were perfused and field stimulated with two pulses at 1 Hz. beta-E depressed stimulation-evoked vasoconstriction with the same potency in both strains. Thus, basal and stress-induced levels of beta-EI did not differ in SHR and WKY. Moreover, in the tail artery of both strains the sensitivity of presynaptic opioid receptors towards beta-E was almost identical. If the beta-E sensitivity of these receptors in other arteries of WKY and SHR is also similar a major role of the circulating peptide in the development of hypertension is rather unlikely.
 ...
PMID:Plasma concentration and vascular effect of beta-endorphin in spontaneously hypertensive and Wistar Kyoto rats. 303 90

Because chronic infusions of adrenalin (A) produce hypertension in rats, it has been suggested that A is a mediator of stress-induced hypertension. In order to test the hypothesis that lowering A will attenuate stress-induced hypertension, rats who had their adrenal medullae removed (ADM) and sham-operated controls were subjected to chronic stress. All subjects were offspring of a cross between spontaneously hypertensive and Wistar-Kyoto rats. Prior to chronic stress, systolic pressures were the same in the two groups. The stress consisted of 60 2-h sessions of shock-shock conflict during 18 weeks. After conflict stress, the rats were implanted with arterial catheters and allowed two days to recover. The resting mean arterial pressure (MAP) was 141.2 mmHg in the ADM group and 142.3 mmHg in the Sham group. Cardiovascular responses to acute stress were then examined. The rats were transferred to a test-box and subjected to pulsed foot shocks (0.5-s duration, 5-s intervals) for 5 min. The MAP increase after transfer was 22.3% in the ADM and 4.2% in the Shams (P less than 0.001). After termination of the shocks, the MAP was elevated 22.2% above baseline in the ADM and 8.1% in the Shams (P less than 0.02). Five minutes after foot shocks the MAP increase was 21.6% in the ADM and 7.2% in the Shams (P less than 0.02). Adrenal demedullation was effective in attenuating plasma A during stress and reduced the plasma noradrenaline response. Therefore, the larger pressor responses of the ADM group seem to result from attenuation of beta-adrenoreceptor-mediated dilation of skeletal muscle vasculature.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Effects of adrenal demedullation on stress-induced hypertension and cardiovascular responses to acute stress. 322 33


1 2 3 4 5 6 7 8 Next >>