Anatomically, the main lumen of the vascular system derives from three layers. The tunica media is the outer layer of tissue and is composed primarily of connective tissue that creates a “tongue-like” appearance on an arterial or venous wall. The tunica adventitia is the innermost layer of vessel wall, comprised primarily by endothelial cells.The tunica intima lies between these two layers and contains blood vessels that are perforated with holes called arteriole or venule ends. (See Figure 1 “Schematic of Layers of Circulation”.)
Most vessel segments are lined with smooth muscle cells (SMCs), which contract to constrict blood flow, thus preventing fluid from passing through the lumen. Smooth muscle is also responsible for maintaining vessel tone – that is, for non-elastic deformation of the vessel wall during and after contraction. In addition, SMCs interact with other cell types to produce the enzyme myosin, which makes the actin filaments within them contract.
In vessels whose diameter is not too large or not too small, arterial and venous walls are like two pieces of gum stuck together: one piece sticks to the inside surface of another. Therefore, one does not feel the walls of the vessel. The vessel that is stuck at the outside surface is called the tunica adventitia and (by default) the vessel that extends to the inside surface is called the tunica intima. This brings up an interesting concept in terms of this explanation: it is much easier to feel a wall by touching its outermost layer than it is to feel a wall by touching its innermost layer. This phenomenon will be significant when considering arterial and venous pressure.
Myosin is needed to cause a muscle cell to contract, and myosin is produced in the smooth muscle cells of arterial and venous walls. Myosin may also be referred to as actin, which is the protein that myosin binds with in order to produce contraction. Myosin molecules are “activated” when calcium ions bind, but they are deactivated once they bind with ADP (adenosine diphosphate). This causes relaxation of the vascular wall. Therefore, calcium ions can be used as a trigger to regulate the diameter of the lumen. When calcium ions are low, smooth muscle cells in the lumen are likely to be contracted. However, when calcium ions are high, smooth muscle cells in the lumen are likely to be relaxed. The reason for this is that myosin is activated when calcium ions bind; therefore, when calcium ions are high (or low), myosin should not be active unless it is bound to actin filaments.
The “trigger” for arterial and venous contraction or relaxation is different from that of skeletal muscle cells. In arterial and venous smooth muscle cells, myosin is activated by adenosine diphosphate (ADP). The concentration of calcium ions in arterial and venous walls is extremely low; therefore, these cells cannot contract unless they have been “triggered”. “Triggering” is accomplished by an increase or decrease in the concentration of ADP. This means that when ADP levels go up or down by a certain amount, myosin will be activated and contraction and relaxation will occur. These changes cause the wall to be rigid at a given level of pressure (when the pressure is high or low). The amount of time that it takes for the vessel to go from collapsed to fully dilated is called the time constant, which in venous vessels is short (0.5 seconds), but in arterial vessels is long (2 seconds). The reason for this phenomenon will be explained further on in this paper.
It may seem as though changing the concentration of ADP will be difficult, since it comes from metabolism – when glucose is broken down into carbon dioxide and water; when fats are broken down into fatty acids and glycerol; and when proteins are broken down into amino acids. Since these reactions take place constantly, the concentration of ADP should always be fairly constant.
