Ways of preventing injury to the endothelium
Controlling your high blood pressure
In the study of Preston, RA et al, titled “Effects of severe hypertension on endothelial and platelet microparticles”, two markers were used to find out if indeed hypertension injures the endothelium. One of these markers is called endothelial microparticles (EMP), and it is released in the bloodstream when the lining of the endothelium is damaged or destroyed. In this study, investigators found out that EMP was very much elevated in the subjects with high blood pressure. This shows that existing high blood pressure could continually and inevitably injure your endothelium, and there is an urgent need to control it.
There is therefore a need to see your medical doctor soonest to control your high blood pressure. If synthetic drugs will be prescribed to you, the drug of choice should be any one belonging to the class of angiotensin-converting enzyme (ACE) inhibitors, because this has been shown to contribute in the restoration of good endothelial function . Examples of generic names belonging to this classare captopril, perindopril, imidapril, and many more. The generic names underthis class of drugs end in “pril”. Thus, if you have elevated level of LDL-cholesterol, in addition to having high blood pressure, ensure that yourmedical doctor prescribes you with any pill belonging to this class of anti-hypertensive drug.
Correcting yourhigh level of LDL-cholesterol
It has been reported that if the level of your LDL-cholesterol is very much above the normal ranges, that the production of nitric oxide (NO) by your endotheliumwill be reduced. When this takes place, the following complications will follow:
Since NO is responsible for the dilation of your blood vessels, the arteries in particular, its low level will lead to the elevation of your blood pressure, since the constriction of your arteries will predominate.
Platelets clump and attach themselves in the endothelial injury
In your blood, there are three types of cells: (1) white blood cells, (2) red blood cells, and (3) platelets. The platelets play a significant role in the formation of blood clots which serve as plugs to any cut in your arm, legs, or in any external part of your body. Without platelets, it is difficult to stop any form of bleeding. When the level of NO in your blood is very much reduced, theplateletseasily form a clump and attach themselves at the injured site in your endothelium forming the so-called plaques which eventually block your arteries and make them inelastic.
This change in the properties of platelets was also shown in the study of Preston, RA et al as stated in the preceding wherein platelet microparticles (PMP) were elevated in subjects whose blood pressure was very high, indicating that platelets have changed in their biological behavior. It is possible that low NO initiates this change in the platelets, and severe hypertension aggravates it.
Smooth muscle cells grow in number and migrate
Your smooth muscle cells which compose the walls of your blood vessels are well-behaved when the level of NO in your blood is normal. However, when its level decreases as a result of having elevated LDL-cholesterol in your blood, your smooth muscle cells become active and aggressive, such that they go out of their way and go to other places which normally are not their territories. They cannot be controlled, and they go astray! Consequently, even in the lining of your endothelium which is in intimate contact with your flowing blood, they grow and invade. These seemingly foreign invaders make your endothelium thicker and more inelastic leading to the development of atherosclerosis and hypertension.
(To be continued)
- Preston RA, WencheJy, Jimenez, JJ, Mauro, LM, Horstman, LL, Valle, M, Aime, G, and Ahn, YS. Effects of severe hypertension on endothelial and platelet microparticles. Hypertension. 2003;41:211-217. doi: 10.1161/01.HYP.0000049760.15764.2D.
- Davigon J, Ganz, Peter. Atherosclerosis: evolving vascular biology and clinical implications, role of endothelial dysfunction in atherosclerosis. Circulation. 2004;109: III-27-III-32. doi:10.1161/01.CIR. 0000131515.03336.f8.