A gene-environment interaction model of stress-induced hypertension

Ikhide G. Imumorin, Yanbin Dong, Haidong Zhu, Joseph C. Poole, Gregory A Harshfield, Frank A. Treiber, Harold Snieder

Research output: Contribution to journalReview article

39 Citations (Scopus)

Abstract

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.

Original languageEnglish (US)
Pages (from-to)109-132
Number of pages24
JournalCardiovascular Toxicology
Volume5
Issue number2
DOIs
StatePublished - Aug 9 2005

Fingerprint

Gene-Environment Interaction
Genes
Hypertension
Neurology
Cardiovascular Models
Sodium
Pituitary-Adrenal System
Parasympathetic Nervous System
Kidney
Sympathetic Nervous System
Primary Prevention
Renin-Angiotensin System
Secondary Prevention
Psychological Stress
Essential Hypertension
Life Style
Angiotensins
Aldosterone
Renin
Phenotype

Keywords

  • Essential hypertension
  • Gene-environment interaction
  • Genetics
  • Stress

ASJC Scopus subject areas

  • Toxicology
  • Cardiology and Cardiovascular Medicine

Cite this

A gene-environment interaction model of stress-induced hypertension. / Imumorin, Ikhide G.; Dong, Yanbin; Zhu, Haidong; Poole, Joseph C.; Harshfield, Gregory A; Treiber, Frank A.; Snieder, Harold.

In: Cardiovascular Toxicology, Vol. 5, No. 2, 09.08.2005, p. 109-132.

Research output: Contribution to journalReview article

Imumorin, Ikhide G. ; Dong, Yanbin ; Zhu, Haidong ; Poole, Joseph C. ; Harshfield, Gregory A ; Treiber, Frank A. ; Snieder, Harold. / A gene-environment interaction model of stress-induced hypertension. In: Cardiovascular Toxicology. 2005 ; Vol. 5, No. 2. pp. 109-132.
@article{a427dc6572c04f4da0f16f0ad325026e,
title = "A gene-environment interaction model of stress-induced hypertension",
abstract = "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.",
keywords = "Essential hypertension, Gene-environment interaction, Genetics, Stress",
author = "Imumorin, {Ikhide G.} and Yanbin Dong and Haidong Zhu and Poole, {Joseph C.} and Harshfield, {Gregory A} and Treiber, {Frank A.} and Harold Snieder",
year = "2005",
month = "8",
day = "9",
doi = "10.1385/CT:5:2:109",
language = "English (US)",
volume = "5",
pages = "109--132",
journal = "Cardiovascular Toxicology",
issn = "1530-7905",
publisher = "Humana Press",
number = "2",

}

TY - JOUR

T1 - A gene-environment interaction model of stress-induced hypertension

AU - Imumorin, Ikhide G.

AU - Dong, Yanbin

AU - Zhu, Haidong

AU - Poole, Joseph C.

AU - Harshfield, Gregory A

AU - Treiber, Frank A.

AU - Snieder, Harold

PY - 2005/8/9

Y1 - 2005/8/9

N2 - 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.

AB - 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.

KW - Essential hypertension

KW - Gene-environment interaction

KW - Genetics

KW - Stress

UR - http://www.scopus.com/inward/record.url?scp=23044500298&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=23044500298&partnerID=8YFLogxK

U2 - 10.1385/CT:5:2:109

DO - 10.1385/CT:5:2:109

M3 - Review article

C2 - 16046788

AN - SCOPUS:23044500298

VL - 5

SP - 109

EP - 132

JO - Cardiovascular Toxicology

JF - Cardiovascular Toxicology

SN - 1530-7905

IS - 2

ER -