Difference between revisions of "Event:937"

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!Event Type
 
!Event Type
 
!Essentiality
 
!Essentiality
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|[[Aop:149|Oxidative Stress Leading to Hypertension]]||KE||[[Aop:149#Essentiality of the Key Events|Strong]]
  
 
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!Evidence
 
!Evidence
 
!Links
 
!Links
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|Homo sapiens||Homo sapiens||[[Event:937#Evidence Supporting Taxonomic Applicability|Strong]]||[http://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi?mode=Info&id=9606 NCBI]
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|Oryctolagus cuniculus||Oryctolagus cuniculus||[[Event:937#Evidence Supporting Taxonomic Applicability|Weak]]||[http://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi?mode=Info&id=9986 NCBI]
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|Mus musculus||Mus musculus||[[Event:937#Evidence Supporting Taxonomic Applicability|Moderate]]||[http://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi?mode=Info&id=10090 NCBI]
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|Rattus norvegicus||Rattus norvegicus||[[Event:937#Evidence Supporting Taxonomic Applicability|Moderate]]||[http://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi?mode=Info&id=10116 NCBI]
  
 
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!Biological Organization
 
!Biological Organization
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|Organ
  
 
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== How this Key Event works ==
 
== How this Key Event works ==
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Vasodilation refers to the widening or increase in the diameter of blood vessels (e.g. large arteries, large veins, small arterioles) that is caused by the relaxation of vascular smooth muscle cells (VSMCs) within the walls of blood vessels, thus increasing blood flow and decreasing arterial blood pressure and heart rate (Siddiqui, 2011). VSMC relaxation is regulated through a number of mechanisms, including cyclic GMP-dependent hyperpolarization and relaxation via nitric oxide (NO), cAMP-dependent hyperpolarization via prostaglandins, and stimulation of potassium channels via endothelial-derived hyperpolarizing factors (Durand and Gutterman, 2013). Under oxidative stress, decreased NO bioavailability results in impaired vasodilation, which is associated with cardiovascular diseases such as hypertension (Silva et al., 2012).
  
 
== How it is Measured or Detected ==
 
== How it is Measured or Detected ==
<em>
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Endothelium-dependent vasodilation can be measured using invasive and non-invasive methods (Raitakari and Celermajer, 2000). For the invasive approach, vasodilation is measured after intra-arterial pharmacologic stimulation with substances that enhance NO release (e.g. acetylcholine, bradykinin). The non-invasive ultrasound-based method evaluates flow-mediated vasodilation (FMD) in the superficial arteries, such as brachial, radial, or femoral vessels.
Methods that have been previously reviewed and approved by a recognized authority should be included in the Overview section above.
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All other methods, including those well established in the published literature, should be described here.  
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Consider the following criteria when describing each method:
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1. Is the assay fit for purpose?
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2. Is the assay directly or indirectly (i.e. a surrogate) related to a key event relevant to the final
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adverse effect in question?
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3. Is the assay repeatable?
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4. Is the assay reproducible?
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</em>
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== Evidence Supporting Taxonomic Applicability ==
 
== Evidence Supporting Taxonomic Applicability ==
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Vasodilation has been observed in humans, rabbits, mice and rats.
  
 
== References ==
 
== References ==
  
 
<references />
 
<references />
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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.
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Raitakari, O.T., and Celermajer, D.S. (2000). Flow-mediated dilatation. Br. J. Clin. Pharmacol. 50, 397–404.
 +
 +
Siddiqui, A. (2011). Effects of Vasodilation and Arterial Resistance on Cardiac Output. J. Clin. Exp. Cardiol. 02.
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 +
Silva, B.R., Pernomian, L., and Bendhack, L.M. (2012). Contribution of oxidative stress to endothelial dysfunction in hypertension. Front. Physiol. 3, 441.

Latest revision as of 13:51, 2 July 2016


Event Title

Vasodilation, impaired

Key Event Overview

Please follow link to widget page to edit this section.

If you manually enter text in this section, it will get automatically altered or deleted in subsequent edits using the widgets.

AOPs Including This Key Event

AOP Name Event Type Essentiality
Oxidative Stress Leading to Hypertension KE Strong

Taxonomic Applicability

Name Scientific Name Evidence Links
Homo sapiens Homo sapiens Strong NCBI
Oryctolagus cuniculus Oryctolagus cuniculus Weak NCBI
Mus musculus Mus musculus Moderate NCBI
Rattus norvegicus Rattus norvegicus Moderate NCBI

Level of Biological Organization

Biological Organization
Organ

How this Key Event works

Vasodilation refers to the widening or increase in the diameter of blood vessels (e.g. large arteries, large veins, small arterioles) that is caused by the relaxation of vascular smooth muscle cells (VSMCs) within the walls of blood vessels, thus increasing blood flow and decreasing arterial blood pressure and heart rate (Siddiqui, 2011). VSMC relaxation is regulated through a number of mechanisms, including cyclic GMP-dependent hyperpolarization and relaxation via nitric oxide (NO), cAMP-dependent hyperpolarization via prostaglandins, and stimulation of potassium channels via endothelial-derived hyperpolarizing factors (Durand and Gutterman, 2013). Under oxidative stress, decreased NO bioavailability results in impaired vasodilation, which is associated with cardiovascular diseases such as hypertension (Silva et al., 2012).

How it is Measured or Detected

Endothelium-dependent vasodilation can be measured using invasive and non-invasive methods (Raitakari and Celermajer, 2000). For the invasive approach, vasodilation is measured after intra-arterial pharmacologic stimulation with substances that enhance NO release (e.g. acetylcholine, bradykinin). The non-invasive ultrasound-based method evaluates flow-mediated vasodilation (FMD) in the superficial arteries, such as brachial, radial, or femoral vessels.

Evidence Supporting Taxonomic Applicability

Vasodilation has been observed in humans, rabbits, mice and rats.

References

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.

Raitakari, O.T., and Celermajer, D.S. (2000). Flow-mediated dilatation. Br. J. Clin. Pharmacol. 50, 397–404.

Siddiqui, A. (2011). Effects of Vasodilation and Arterial Resistance on Cardiac Output. J. Clin. Exp. Cardiol. 02.

Silva, B.R., Pernomian, L., and Bendhack, L.M. (2012). Contribution of oxidative stress to endothelial dysfunction in hypertension. Front. Physiol. 3, 441.