Cardiovascular Reactivity in Youth

Treiber, Frank A.; Snieder, Harold

doi:10.1007/978-1-59259-797-0_14

Cited by 2 publications

(2 citation statements)

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“…Based on the findings of this study and recent reports associating stress-induced U Na V with left ventricular structure 5, cardiovascular load 4, adiposity 50–52 and a higher albumin excretion rate 6, we propose the further use of ΔU Na V and stress U Na V as heritable intermediate phenotypes in genetic studies on the early development of stress-induced essential hypertension. 3,7,8 Future identification of the genes responsible for SIPN heritability will help elucidate the contribution of stress in combination with genetic susceptibility in the development of essential hypertension.…”

Section: Discussionmentioning

confidence: 99%

“…3,7,8 Several studies suggest the importance of genetic influence on renal handling of sodium, but evidence is indirect with regard to the renal response to stress. 3 For example, the heritability of salt sensitivity, defined as an increased BP response to high-salt intake or decrease of BP on a low-salt diet 9 has been well-documented 10–13 and heritabilities between 43% and 52% have been observed for fractional and 24-h sodium excretion.…”

Section: Introductionmentioning

confidence: 99%

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Stress-Induced Sodium Excretion

Zhu

et al. 2009

Hypertension

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Abstract-Impaired stress-induced pressure natriuresis, ie, an inadequate compensatory increase in urinary sodium excretion (U Na V) in response to a stress-induced blood pressure increase, may lead to the premature development of essential hypertension. To assess the heritability of baseline U Na V, stress U Na V, and the U Na V response to stress (⌬U Na Vϭstress U Na VϪ baseline U Na V), we studied 396 black and 494 white twins, including monozygotic and dizygotic twins of the same as well as the opposite sex (mean age: 17.6Ϯ3.3 years; range: 11.9 to 30.0 years). Bivariate genetic model fitting was performed to examine the extent to which genetic and environmental factors are common or specific to baseline and stress U Na V. Heritability estimates for ⌬U Na V can be derived from these bivariate models. All of the bivariate analyses were performed separately in whites and blacks, because univariate models for baseline U Na V showed significant ethnic differences in heritability estimates. Best-fitting models showed that the heritability of stress U Na V was 0.42 in whites and 0.58 in blacks. Only 15% and 11% of the total variance could be attributed to genetic factors common to baseline and stress U Na V in whites and blacks, respectively. After removal of all of the shared influences with baseline U Na V, heritabilities for stress U Na V were 0.32 in whites and 0.57 in blacks. Heritability estimates for ⌬U Na V were 0.36 in whites and 0.39 in blacks. In summary, this study establishes ⌬U Na V and stress U Na V as heritable phenotypes that may be used to study the genetic etiology of early hypertension development. Key Words: natriuresis Ⅲ blood pressure Ⅲ risk factors Ⅲ genetics Ⅲ twin study Ⅲ black T he key role of the kidney in long-term blood pressure (BP) regulation is generally recognized 1,2 and includes sodium handling in response to extended periods of stress. 3 We showed recently that individuals without an adequate compensatory increase in the urinary sodium excretion (U Na V) rate in response to a stress-induced BP increase (ie, impaired stress-induced pressure natriuresis [SIPN]) show a delayed BP recovery after stress, which seemed to be at least partly because of their increased blood volume. 4 For the same level of stress, individuals who show impaired SIPN are, therefore, exposed to a greater cardiovascular and renal load, which may lead to the premature development of essential hypertension and its sequelae. 4,5 This scenario was supported by a recent study in which we observed that adolescent black subjects with impaired SIPN showed a higher albumin excretion rate than those with normal sodium excretion. 6 We previously proposed a gene-environment interaction model of stress-induced hypertension in which we integrated both short-term (cardiovascular) and long-term (renal) BP regulatory pathways. 3,7,8 Several studies suggest the importance of genetic influence on the renal handling of sodium, but evidence is indirect with regard to the renal response to stress. 3 For example, the heritability ...

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Stress-Induced Sodium Excretion

Zhu

et al. 2009

Hypertension

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A Gene–Environment Interaction Model of Stress-Induced Hypertension

Imumorin

Dong

Zhu

et al. 2005

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The case for a gene-environment interaction model of stress-induced hypertension is detailed in this paper. We hypothesize that repeated exposure to stress in combination with an environmentally and/or genetically mediated susceptibility may lead to the development of essential hypertension. Previously, we reviewed the evidence for a genetic influence on the two major intermediate phenotypes of our model: cardiovascular reactivity to psychological stress and stress-induced sodium retention, representing the cardiovascular and renal stress response, respectively. Here we first describe how genes underlying the physiological systems mediating the stress response of heart, vasculature, and kidney (i.e., the sympathetic nervous system, renin-angiotensin- aldosterone system and sodium reabsorption, and the endothelial system) may increase vulnerability to stress and confer susceptibility to development of essential hypertension. Next, we extend our model and review genes underlying three additional systems that may mediate the influence of stress on the development of essential hypertension: the parasympathetic nervous system, the serotonergic system, and the hypothamamus-pituitary-adrenal axis. The elucidation of our gene-environment interaction model of stress-induced essential hypertension will improve the understanding of the contribution of stress to the development of essential hypertension. This knowledge may lead to more effective primary and secondary prevention programs involving lifestyle interventions in which the role of stress, both acute and chronic, will be taken into account, particularly for individuals at increased genetic risk of essential hypertension.

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Cardiovascular Reactivity in Youth

Cited by 2 publications

References 91 publications

Stress-Induced Sodium Excretion

Stress-Induced Sodium Excretion

A Gene–Environment Interaction Model of Stress-Induced Hypertension

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