Role of Cardiovascular Reactivity to Mental Stress in Predicting Future Hypertension

Bedi, Mona; Varshney, Vaibhav Kumar; Babbar, Rashmi

doi:10.1081/ceh-100100058

Cited by 31 publications

(29 citation statements)

References 91 publications

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“…Reactivity-induced changes in the laboratory are of interest because they have been found to be predictive of future cardiovascular events, e.g. larger transient increases in blood pressure responses to stressors have been associated with the development of fixed hypertension [60][61][62][63]. Psychological and exercise challenges lead to increased cytokine levels, the increased expression of cellular adhesion molecules CD11a and CD11b on PBMC, increased soluble adhesion molecule sICAM-1, and increased PBMC chemotaxis [58,59,[64][65][66].…”

Section: Responses To Stressors and Inflammation In Hypertensionmentioning

confidence: 97%

The potential anti-inflammatory benefits of improving physical fitness in hypertension

Edwards¹,

Mills²

2007

Journal of Hypertension

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Hypertension is associated with an increased risk of stroke and atherosclerosis. In addition to elevated blood pressure, hypertension is characterized by neuroendocrine and immune activation, including elevated levels of C-reactive protein, inflammatory cytokines, and soluble adhesion molecules, which are predictive of morbidity and mortality outcomes. Pharmacological treatment for hypertension reduces blood pressure, but has limited effectiveness in reducing the accompanying inflammation and its associated morbidity and mortality. Exercise and diet interventions regularly show reductions in blood pressure in hypertensive individuals. Similar interventions in other populations show reductions in many inflammatory markers, but these effects have not been routinely examined in hypertensive individuals. The mechanisms through which exercise might exert an anti-inflammatory action include the sympathetic nervous system, the hypothalamic-pituitary-adrenal axis, as well as direct effects of blood pressure. Here, exercise is promoted as a potentially effective treatment for both the elevated blood pressure and chronic inflammation found in hypertension.

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Section: Responses To Stressors and Inflammation In Hypertensionmentioning

confidence: 97%

The potential anti-inflammatory benefits of improving physical fitness in hypertension

Edwards¹,

Mills²

2007

Journal of Hypertension

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“…According to the reactivity hypothesis, supported by several investigators, 9 the increase of pressure response to the stimuli is considered to be a factor in precipitating and perpetuating hypertension, but the aetiological role of cardiovascular reactivity in the development of hypertension has not been resolved. 10 Hypertensive subjects exhibit larger BP and HR responses during the tasks than the normotensive subjects, even when borderline or mildly hypertensives have been studied. 11 A relation between an exaggerated response of BP to mental stress tasks and subsequent BP status has been observed in some prospective studies.…”

Section: Introductionmentioning

confidence: 97%

Blood pressure reactivity to mental stress task as a determinant of sustained hypertension after 5 years of follow-up

et al. 2003

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Previous studies have reported an increased risk of developing sustained hypertension (SH) in borderline or mildly hypertensive subjects showing an exaggerated response of blood pressure (BP) to mental stress. The aim of this study was to assess if the response of BP to mental stress tasks is an independent predictor of SH. A total of 89 patients with grade 1 hypertension, aged 18-64 years, 62% males, were included. The mean of follow-up was 5.3 years (s.d. 2.1 years). SH was defined as the development of grades 2-3 hypertension (Systolic BPX160 mmHg or diastolic BPX100 mmHg) or to be in antihypertensive treatment after follow-up. Two mental stress tasks: mental arithmetic stress task and a stressful interview (SI) were applied at entry. The subjects were classified as hyper-reactors when BP increase was greater than 35 mmHg for systolic BP or greater than 21 mmHg for diastolic BP, according to the results obtained previously in a normotensive control group. In the univariate analysis, the factors associated with the development of SH were age (P ¼ 0.0007), office diastolic BP (P ¼ 0.014) and hyper-reactivity of BP during a stressful interview (P ¼ 0.003). In the Cox regression model, after adjusting for gender, age, and office BP, the hyper-reactivity of BP during SI was an independent predictor of development of SH. In conclusion, the response of BP to mental stress tasks is useful in predicting SH in young and middle-aged subjects with grade 1 hypertension.

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“…PSYCHOSOCIAL STRESS INCREASES arterial pressure and also has been linked to chronic renal and cardiovascular disease, including hypertension (1,9,17,19). Stress causes activation of the sympathetic nervous system (SNS) and the hypothalamicpituitary-adrenocortical axis, with responses that include increases in body temperature, blood pressure, heart rate (HR), and plasma glucocorticoid concentration.…”

mentioning

confidence: 99%

“…The later phase of the pressor response is blocked similarly by a ␤1-receptor antagonist and an ACE inhibitor, independent of HR, suggesting that the ␤1-dependent blood pressure effect is due, in large part, to the renin-angiotensin system. mean arterial pressure; sympathetic nervous system; renin-angiotensin system PSYCHOSOCIAL STRESS INCREASES arterial pressure and also has been linked to chronic renal and cardiovascular disease, including hypertension (1,9,17,19). Stress causes activation of the sympathetic nervous system (SNS) and the hypothalamicpituitary-adrenocortical axis, with responses that include increases in body temperature, blood pressure, heart rate (HR), and plasma glucocorticoid concentration.…”

mentioning

confidence: 99%

Sympathetic and angiotensin-dependent hypertension during cage-switch stress in mice

Lee¹,

Webb²,

Brands³

2004

American Journal of Physiology-Regulatory, Integrative and Comp

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Lee, Dexter L., R. Clinton Webb, and Michael W. Brands. Sympathetic and angiotensin-dependent hypertension during cageswitch stress in mice. Am J Physiol Regul Integr Comp Physiol 287: R1394 -R1398, 2004. First published August 12, 2004 doi:10.1152/ ajpregu.00306.2004.-The goal of this study was to determine the dependence of the acute hypertensive response to a novel model of acute psychosocial stress on the sympathetic and renin-angiotensin systems. Baseline mean arterial pressure (MAP), heart rate (HR), and locomotor activity were measured with telemetry in mice for a 1-h period and averaged 98 Ϯ 1 mmHg, 505 Ϯ 3 beats/min, and 5 Ϯ 1 counts, respectively. Stress was induced by placing a mouse into a cage previously occupied by a different male mouse, and this increased MAP, HR, and activity in the control group by 40 Ϯ 2 mmHg, 204 Ϯ 25 beats/min, and 68 Ϯ 6 counts, respectively. Each variable gradually returned to baseline levels by 90 min after beginning cage switch. Pretreatment with terazosin (10 mg/kg ip) significantly reduced the initial increase in MAP to 12 Ϯ 6 mmHg, whereas MAP for the last 45 min was superimposable on control values. Atenolol (10 mg/ml drinking water) had no effect to blunt the initial increase in MAP but had a growing effect from 10 min onward, decreasing MAP all the way to baseline by 60 min after starting cage switch. Captopril (2 mg/ml drinking water) treatment caused a very similar response. All three treatments significantly decreased the area under the blood pressure curve, and the blood pressure effect could not be attributed uniformly to effects on HR or activity. These data suggest that our novel model of psychosocial stress causes an initial ␣1-receptordependent increase in MAP. The later phase of the pressor response is blocked similarly by a ␤1-receptor antagonist and an ACE inhibitor, independent of HR, suggesting that the ␤1-dependent blood pressure effect is due, in large part, to the renin-angiotensin system. mean arterial pressure; sympathetic nervous system; renin-angiotensin system PSYCHOSOCIAL STRESS INCREASES arterial pressure and also has been linked to chronic renal and cardiovascular disease, including hypertension (1,9,17,19). Stress causes activation of the sympathetic nervous system (SNS) and the hypothalamicpituitary-adrenocortical axis, with responses that include increases in body temperature, blood pressure, heart rate (HR), and plasma glucocorticoid concentration. Interference with either system compromises the body's ability to respond to the stressors (2,16,20). The well-described effects of the SNS are mediated through ␣-and ␤-adrenergic receptors located on the heart and throughout the vascular system, which includes the stimulation of renin secretion and subsequent increase in ANG II production (3,4,7,8,10,18).We have a new experimental model of psychosocial stress that is caused by placing a male mouse in a cage previously occupied by another male mouse. Termed cage switch (CS), this is a modification of earlier models of stress, in which rats ...

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Role of Cardiovascular Reactivity to Mental Stress in Predicting Future Hypertension

Cited by 31 publications

References 91 publications

The potential anti-inflammatory benefits of improving physical fitness in hypertension

The potential anti-inflammatory benefits of improving physical fitness in hypertension

Blood pressure reactivity to mental stress task as a determinant of sustained hypertension after 5 years of follow-up

Sympathetic and angiotensin-dependent hypertension during cage-switch stress in mice

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