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Key Event Title
Key Event Components
Key Event Overview
AOPs Including This Key Event
|All life stages||High|
Key Event Description
Hypertension is an important cardiovascular risk factor and considered one of the leading causes of cardiovascular morbidity and mortality (Kizhakekuttu and Widlansky, 2010). It is defined as a chronic elevation in blood pressure and is characterized by elevated systemic vascular resistance due to dysregulated vasomotor function and structural remodeling (Lee and Griendling, 2008). Although many genetic and environmental factors contribute to the development to hypertension, oxidative stress appears to be the main pathway involved in its pathogenesis. Excessive reactive oxygen species (ROS) contributes to endothelial nitric oxide synthase (eNOS) uncoupling, resulting in increased superoxide production but decreased nitric oxide (NO), a critical regulator of vascular homeostasis (Silva et al., 2012). Depletion of NO leads to impaired endothelium-dependent vasodilation, thus promoting endothelial dysfunction, which is a hallmark of hypertension.
How It Is Measured or Detected
Arterial blood pressure is commonly measured using a sphygmomanometer, which provides systolic and diastolic blood pressure measurements in millimeters of mercury (mmHg).
Pathological hypertension is characterised according to current guidelines; https://www.nice.org.uk/guidance/cg127/evidence
Stage 1 hypertension : Clinic blood pressure is 140/90 mmHg or higher and subsequent ambulatory blood pressure monitoring (ABPM) daytime average or home blood pressure monitoring (HBPM) average blood pressure is 135/85 mmHg or higher.
Stage 2 hypertension : Clinic blood pressure is 160/100 mmHg or higher and subsequent ABPM daytime average or HBPM average blood pressure is 150/95 mmHg or higher.
Severe hypertension : Clinic systolic blood pressure is 180 mmHg or higher or clinic diastolic blood pressure is 110 mmHg or higher.
Domain of Applicability
Animal models including mouse and rat models are routinely used to study hypertension, and have been shown to reflect human physiology relating to hypertension (Leong et al., 2015).
Evidence for Perturbation by Stressor
Regulatory Significance of the Adverse Outcome
Durand, M.J., and Gutterman, D.D. (2013). Diversity in mechanisms of endothelium-dependent vasodilation in health and disease. Microcirc. N. Y. N 1994 20, 239–247.
Kizhakekuttu, T.J., and Widlansky, M.E. (2010). Natural antioxidants and hypertension: promise and challenges. Cardiovasc. Ther. 28, e20–e32.
Leong, X.-F., Ng, C.-Y., Jaarin, K., Leong, X.-F., Ng, C.-Y., and Jaarin, K. (2015). Animal Models in Cardiovascular Research: Hypertension and Atherosclerosis, Animal Models in Cardiovascular Research: Hypertension and Atherosclerosis. BioMed Res. Int. BioMed Res. Int. 2015, 2015, e528757.
Silva, B.R., Pernomian, L., and Bendhack, L.M. (2012). Contribution of oxidative stress to endothelial dysfunction in hypertension. Front. Physiol. 3, 441.