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Event: 952

Key Event Title

A descriptive phrase which defines a discrete biological change that can be measured. More help

Hypertension

Short name
The KE short name should be a reasonable abbreviation of the KE title and is used in labelling this object throughout the AOP-Wiki. More help
Hypertension
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Biological Context

Structured terms, selected from a drop-down menu, are used to identify the level of biological organization for each KE. More help
Level of Biological Organization
Individual

Key Event Components

The KE, as defined by a set structured ontology terms consisting of a biological process, object, and action with each term originating from one of 14 biological ontologies (Ives, et al., 2017; https://aopwiki.org/info_pages/2/info_linked_pages/7#List). Biological process describes dynamics of the underlying biological system (e.g., receptor signalling).Biological process describes dynamics of the underlying biological system (e.g., receptor signaling).  The biological object is the subject of the perturbation (e.g., a specific biological receptor that is activated or inhibited). Action represents the direction of perturbation of this system (generally increased or decreased; e.g., ‘decreased’ in the case of a receptor that is inhibited to indicate a decrease in the signaling by that receptor).  Note that when editing Event Components, clicking an existing Event Component from the Suggestions menu will autopopulate these fields, along with their source ID and description.  To clear any fields before submitting the event component, use the 'Clear process,' 'Clear object,' or 'Clear action' buttons.  If a desired term does not exist, a new term request may be made via Term Requests.  Event components may not be edited; to edit an event component, remove the existing event component and create a new one using the terms that you wish to add.  Further information on Event Components and Biological Context may be viewed on the attached pdf. More help
Process Object Action
hypertension increased

Key Event Overview

AOPs Including This Key Event

All of the AOPs that are linked to this KE will automatically be listed in this subsection. This table can be particularly useful for derivation of AOP networks including the KE.Clicking on the name of the AOP will bring you to the individual page for that AOP. More help
AOP Name Role of event in AOP Point of Contact Author Status OECD Status
Hypertension AdverseOutcome Brendan Ferreri-Hanberry (send email) Not under active development Under Development
Na+ /K+ -ATPase inhibition leading to hypertension AdverseOutcome Allie Always (send email) Under development: Not open for comment. Do not cite

Taxonomic Applicability

Latin or common names of a species or broader taxonomic grouping (e.g., class, order, family) that help to define the biological applicability domain of the KE.In many cases, individual species identified in these structured fields will be those for which the strongest evidence used in constructing the AOP was available in relation to this KE. More help
Term Scientific Term Evidence Link
Homo sapiens Homo sapiens High NCBI
Mus musculus Mus musculus High NCBI
Rattus norvegicus Rattus norvegicus High NCBI

Life Stages

An indication of the the relevant life stage(s) for this KE. More help
Life stage Evidence
All life stages High

Sex Applicability

An indication of the the relevant sex for this KE. More help
Term Evidence
Unspecific High

Key Event Description

A description of the biological state being observed or measured, the biological compartment in which it is measured, and its general role in the biology should be provided. More help

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

A description of the type(s) of measurements that can be employed to evaluate the KE and the relative level of scientific confidence in those measurements.These can range from citation of specific validated test guidelines, citation of specific methods published in the peer reviewed literature, or outlines of a general protocol or approach (e.g., a protein may be measured by ELISA). Do not provide detailed protocols. More help

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

A description of the scientific basis for the indicated domains of applicability and the WoE calls (if provided).  More help

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).

Regulatory Significance of the Adverse Outcome

An AO is a specialised KE that represents the end (an adverse outcome of regulatory significance) of an AOP. More help

References

List of the literature that was cited for this KE description. More help

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.