What's in a blood vessel?
What's in this diagram?
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In a normal, healthy individual, inner layer (endothelial cells release a messenger molecule (vasodilator NO) which causes smooth muscle cells to dilate. As we age, this function is depleted and our arteries' ability to widen decreases with age.
Figure 1
(Pober et al., 2007). " Functions of resting endothelial cells" Evolving functions of endothelial cells in inflammation.
What's in this diagram?
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When the heart contracts (systole) to push blood out, the arteries can expand and store up pressure, containing some of the blood that is being ejected. On the other hand, when the heart relaxes (diastole), the arteries, can recoil and push blood in the same direction, maintain continuous blood flow and keep pressure within narrow limits.
We all know that blood is life - it provides all our different tissues and organs with oxygen and nutrients. If blood is life, then what is the giver of life? Arteries are. These are the conduits that transport the oxygen dissolved from our lungs to the rest of our body tissues.
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As seen in the video, arteries comprise of several layers
- an outer layer
- smooth muscles
- elastin
- connective tissue
- inner layer/endothelium
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These layers are crucial to maintain arterial elasticity and vasodilation function (explained in further details below)
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Endothelium dependent dilation (EDD)
Smooth muscles are responsible for the widening or constricting of arteries while the inner layer (i.e endothelium) releases molecules known as vasodilators (e.g nitric oxide, NO) that signals smooth muscles to relax for vasodilation. (see figure 1) This is known as endothelial dependent dilation. (EDD) (1)
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Arterial elasticity
Elastin allows arteries to be elastic and connective tissues like collagen gives it strength, but is also responsible for its stiffness. When the heart pushes blood out, the elastic properties of the artery allow it to expand and store up blood. Shortly after, when the heart relaxes, the arteries can recoil and push blood forward to the rest of our tissues (see figure 2) , hence ensuring a continuous flow of blood to tissues and keeping blood pressure within narrow limits. (2)
Figure 2
(Laurent et al., 2020). "Schematic representation of the role of arterial compliance in dampening blood pressure pulsatility and assuring adapted blood flow through the peripheral circulation." Arterial stiffness and hypertension in the elderly.
resource by wix
How do our arteries age?
Endothelium dysfunction
As we age, the endothelium begins to lose its function of releasing vasodilators such as NO, while other molecules which increase in our blood as we age inactivate some of the remaining NO that is released. This reduces the ability of our endothelium to induce dilation in our arteries, hence giving rise to the aging phenomenon known as endothelium dysfunction. This therefore causes problems in regulating blood flow and supply.
Figure 3
(Barbosa et al., 2019). "Multiple causes of arterial stiffness with aging and disease". Arterial stiffness and coronary artery disease.
Figure 4
(Ogola et al., 2018). New insights into arterial stiffening : Does sex matter? A; A healthy artery, B: a stiffened artery
What's in this diagram?
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A represents the healthy arteries during a contraction while B represents stiffened arteries. as can be observed, the healthy arteries store up blood and pressure during a heart contraction while stiffened arteries fail to do so, leading to higher pressure that downstream blood vessels are subjected to (compare size of arrows) This leads to failure to maintain blood flow, fluctuations in blood pressure between heart contractions, and organ damage, causing multiple CVDs
Arterial stiffening
Due to various reasons, the collagen content in our arteries increase with age, while the elastin decreases. This is also characterized by a thickening of the middle layer (media) (see figure 3). The consequence of such arterial stiffening is shown in figure 4. There is a reduced ability to store up pressure and blood volume during a heart contraction, resulting in little control of pressure on blood vessels lying ahead of it. At the same time, no blood volume is stored, affecting its ability to maintain blood flow during systole. This leads to fluctuations in blood pressure, reduced blood flow during heart contractions as well as damage to other organs, causing multiple CVDs and other diseases. (3)
Done by: Timothy Ng
References
1. Pober, J. S., & Sessa, W. C. (2007). Pober JS, Sessa WCEvolving functions of endothelial cells in inflammation. Nat Rev Immunol 7:803-815. Research Gate. https://www.researchgate.net/publication/5950336_Pober_JS_Sessa_WCEvolving_functions_of_endothelial_cells_in_inflammation_Nat_Rev_Immunol_7803-815
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2. Ogola, B. O., Zimmerman, M. A., Clark, G. L., Abshire, C. M., Gentry, K. M., Miller, K. S., & Lindsey, S. H. (2018). New insights into arterial stiffening: Does sex matter? American Journal of Physiology-Heart and Circulatory Physiology, 315(5), H1073–H1087. https://doi.org/10.1152/ajpheart.00132.2018
3.Nowak, K. L., Rossman, M. J., Chonchol, M., & Seals, D. R. (2018). Strategies for achieving healthy vascular aging. Hypertension, 71(3), 389–402. https://doi.org/10.1161/HYPERTENSIONAHA.117.10439
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video:
7activestudio. (2014, May 16). Blood vessels [video]. https://www.youtube.com/watch?v=aVPCP8fzf9c
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image:
Pober, J. S., & Sessa, W. C. (2007). Evolving functions of endothelial cells in inflammation. Nature Reviews Immunology, 7(10), 803‑815. https://doi.org/10.1038/nri2171
Laurent, S., & Boutouyrie, P. (2020). Arterial stiffness and hypertension in the elderly. Frontiers in Cardiovascular Medicine, 7, 202. https://doi.org/10.3389/fcvm.2020.544302
Barbosa, E. (2019). Arterial stiffness and coronary artery disease. Journal of Cardiology & Cardiovascular Therapy, 14(3). https://doi.org/10.19080/JOCCT.2019.14.555889
Ogola, B. O., Zimmerman, M. A., Clark, G. L., Abshire, C. M., Gentry, K. M., Miller, K. S., & Lindsey, S. H. (2018). New insights into arterial stiffening : Does sex matter? American Journal of Physiology-Heart and Circulatory Physiology, 315(5), H1073‑H1087. https://doi.org/10.1152/ajpheart.00132.2018