Key Event Title
Key Event Component
Key Event Overview
AOPs Including This Key Event
|AOP Name||Role of event in AOP|
|Peptide Oxidation Leading to Hypertension||KeyEvent|
Level of Biological Organization
|Homo sapiens||Homo sapiens||Strong||NCBI|
|Oryctolagus cuniculus||Oryctolagus cuniculus||Weak||NCBI|
|Mus musculus||Mus musculus||Moderate||NCBI|
|Rattus norvegicus||Rattus norvegicus||Moderate||NCBI|
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.
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.