Biology:Acute Local Blood Flow Regulation

Acute local blood flow regulation refers to the rapid control of arterial vasomotion usually based on the metabolic needs of the surrounding cells. Although cardiac output may remain the same, blood flow to individual cells is chiefly dependent on the cells' need for nutrients.

For example, during exercise such as running, the metabolic needs of the active leg skeletal muscles increase significantly. The muscle cells are in much more demand for nutrients such as oxygen. However, the body "reserves" as much blood as possible to the active tissues (in this case skeletal muscle). Therefore, during exercise more blood will flow to-and-from the muscle than it will in inactive tissue, such as the hand muscles.

It should also be pointed out that an increase in the diameter of a blood vessel will also increase the volume of blood flow that passes through. More blood flow would also result in a higher concentration of nutrients.

There are currently two major theories of the mechanism behind local control of blood flow. They include the vasodilator theory and the oxygen lack theory.

Vasodilator Theory

According to this theory, the greater the rate of metabolism or the less availability of oxygen or other nutrients to a tissue, the greater the rate of formation of vasodilator metabolites in the tissue cells. These metabolites then are believed to diffuse into the capillary and act upon the precapillary sphincters, metarterioles, and arterioles to cause vasodilation.

Vasodilator substances may be released from the tissue in response to hypoxia. For example, experiments have shown that amounts of both adenosine and lactic acid tend to increase significantly in the interstitial spaces between active skeletal muscle cells. This also results in an acute vasodilation of the arterioles supplying the active tissue.

Many physiologists believe that adenosine is an especially important vasodilator metabolite. For instance, during partial occlusion of a coronary artery, minute amounts of adenosine are released from the nearby cardiac muscle cells, thus restoring blood flow back to normal. Furthermore, during decreased oxygen concentration in the heart the cells begin to degrade adenosine triphosphate, which increases the release of adenosine.

Although nitric oxide also has vasodilator properties, it is not released by the cells during oxygen deprivation. Instead, nitric oxide is released due to excessive shear stress on the arteriole, which is usually an indication of high blood pressure. This results in vasodilation and a decrease in blood pressure. Therefore, nitric oxide is only produced during excessive vasoconstriction as opposed to hypoxia.

Oxygen Lack Theory

This theory, also called the "nutrient demand theory", is based on dilation due to hypoxia of the vascular smooth muscle, not the surrounding cells.

Oxygen (as well as other nutrients) is needed to cause vascular smooth muscle contraction. In fact, at rest the arterioles are normally kept slightly constricted due to the vasomotor tone. Some physiologists theorize that in the absence of adequate amounts of oxygen to the vascular smooth muscle cells, the muscles could not remain contracted and would therefore relax, causing vasodilation.

This theory is less popular than the previously-discussed vasodilator theory. However, it is likely that both of these mechanisms work synergistically as a result of nutrient deprivation or hypoxia.

References

Hall, John. "Local and Humoral Control of Tissue Blood Flow." Guyton and Hall Textbook of Medical Physiology. Philadelphia: 2011.