Anatomy of the blood vessel wall
You have three types of blood vessels: (1) arteries, (2) veins, and (3) capillaries. Your arteries carry the blood from your heart and deliver them to different parts of your body. You veins collect the blood from the different parts of your body and return it to the heart. Your capillaries, on the other hand, connect your network of arteries to your network of veins.In the development of hypertension and heart diseases, the type of blood vessels that are primarily involved are the arteries.Therefore, the center of discussion in the next few sections will be on them.
Your arteries can be likened to your water pipes at home. They are tubes wherein fluid passes through. In your water pipes, water passes through them; in your blood vessels, blood will pass through them. Your arteries are relatively thick tubes, and they are made this way because they need to withstand the high pressure generated by your blood and the regularpumping of your heart.
The wall of your arteries are made up of three layers: (1) tunica adventitia, (2) tunica media, and (3) tunica intima, also known as the endothelium.The tunica adventitia is the outermost layer, the tunica media is the middle layer, and the tunica intima is the innermost layer. The tunica adventitia is responsible for attaching your arteries to the surrounding tissues, thereby preventing them from moving astray. In addition, it provides some strength for your arteries. The tunica media is mainly responsible for providing the strength of your arteries to contain your varying blood pressure. Meanwhile, the tunica intima provides the internal lining of your arteries.
Important role of the tunica intimaor endothelium
Since the tunica intima or endothelium is the innermost lining of your arteries, it is in intimate contact with the flow of your blood. As your blood flows in your arteries, your endothelium offers a frictional resistance to such flow; therefore, the endothelium receives the brunt of the flowing blood. In the parlance of medicine, this is called the shearing effect of the flowing blood. When your blood pressure is very much increased compared to the normal values, this shearing effect also increases, and your endothelium will be injured. The higher the blood pressure is, the higher and more serious the injury to your endothelium will be. This injury will be the beginning of developing the so-called atherosclerosis wherein fatty substances are attached to the lining of the endothelium, giving rise to inelastic arteries which will, in turn, lead to the development of hypertension and heart diseases.
Injury to the endothelium and high level of LDL-cholesterol
In the development of atherosclerosis (deposition of fatty substances in the endothelium), it has been established that the first stage in the process is the infliction of injury to the endothelium.This injury to the endotheliumare caused by increased blood pressure and the increased level of LDL-cholesterol. Hence, if you have elevated blood pressure and you have elevation of the LDL-cholesterol, your hypertension will get worse as days go by, if you do not take medicines to control your high blood pressure and the elevated level of LDL-cholesterol.
The LDL-cholesterol has dual effects in the causation and worsening of atherosclerosis. Firstly, it decreases the production of nitric oxide which is responsible for the dilation of the arteries. Thus, in the absence of nitric oxide, you are prone to have elevated blood pressure because of constriction of your arteries.Secondly, with increased level of LDL-cholesterol in the blood, these fatty substances, together with platelets, could attach themselves in the injured sites in the endothelium. This will make the arteries inelastic and obstructed—be it partial or total—leading to the development of hypertension and heart diseases.
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.