Arterioles are the smallests vessels of the arterial system, with a diameter of about 1/3 millimeter or smaller. There is much smooth muscle in their tunica media, which causes vasocontriction when it contracts, and vasodilation when it relaxes. Such vasoconstriction and vasodilation plays two important roles in the cardiovascular system.
First, let's make a list of the most important factors causing vasoconstriction or vasodilation in arterioles.
LOCAL CHEMICAL FACTORS: In general, as these factors are added to the intersitital fluid in tissues, they cause vasodilation to help match the local blood flow to the local metabolic requirments. These include CO2, H+, K+, adenosine, osmolarity. In each case, increasing levels leads to increased blood flow in the local tissue.
SYMPATHETIC NERVES: Norepinephrine acting on alpha receptors causes vasoconstriction. This effect in strong in the skin, digestive tract and kidneys. In these organs, normal blood flow greatly surpasses that required to keep the tissues alive. Instead, most of the blood flow serves specific physiological functions in the organs. By contrast, such vasoconstriction does does not occur in the brain or heart, where blood flow serves to keep the cells in these vital organs alive and healthy.
NON-ADRENERGIC, NON-CHOLINERGIC AUTONOMIC NERVES: Some autonomic nerves do not release norepinephrine or acetylcholine. Instead they release nitric oxide, which is a vasodilator. This is most important in the digestive tract and penis. Also, as described below, nitric oxide can be released in many places from the endothelial cells.
HORMONES: In the heart, norepinephrine and epinephrine have the same effect since there are only beta receptors. But in blood vessels there can be both alpha receptors, which cause vasoconstriction, and beta-2 receptors, which cause vasodilation. Since epinephrine preferentially activates beta-2 receptors, it can cause vasodilation if there are sufficient beta-2 receptors. This effect is mainly important in skeletal muscles during exercise.
Two hormones that regulate kidney physiology, angiotensin II and vasopressin, are powerful vasoconstrictors. These play an important role in supporting the arterial pressure during serious decreases in the extracellular fluid volume, such as might occur during serious hemorrhage.
PARACRINES: We have already frequently encountered vasodilation caused by inflammatory paracrines. Another important paracrine, nitric oxide, is released by endothelial cells. Some nitric oxide is released continually and plays a role in regulation, for example, in respiratory physiology. More is also released during inflammation.
Now let us see how the above factors control the distribution of blood flow in physiological situations. The structures that normally have the largest changes in blood flow are the skin, the digestive tract and skeletal muscle.
SKIN: Blood flow to the skin is almost entirely for the purposes of thermoregulation. Very little of the total is required to support the metabolism of the skin cells. Heat is carried by the blood from inside the body to the skin, where it is lost to the atmosphere. Most heat is lost this way, with the only other significant loss of heat occurring through breathing. Sympathetic nerves control the skin arterioles for this purpose, with greater release of norepinephrine causing vasoconstriction. Since under neutral conditions there is some steady sympathetic activity to the skin, reduction of the sympathetic effects allows vasodilation. Unlike many structures, arterioles do not have the dual innervation by both sympathetic and parasympathetic nerves.
DIGESTIVE TRACT: As with the skin, most of the blood flow to the digestive tract is not for the purpose of supporting the cells of the digestive tract, but rather, of course, to pick up nutrients absorbed in digestion. Again, sympathetic nerves causing vasoconstriction are the dominant factor here. Removable of the sympathetic effect causes vasodilation. Nitric oxide can play a role here too.
SKELETAL MUSCLE: As a skeletal muscle makes the transition from relaxed to maximum exercise, the blood flow can increase by up to approximately 20 times. There are two factors at work here. At rest, sympathetic nerves constrict the arterioles in muscle. Then as exercise begins, this effect is removed and some vasodilation occurs.
Epinephrine, acting on beta-2 receptors, also can cause vasodilation in skeletal muscle during exercise.
But the greatest subsequent vasodilation is due to local chemical factors . These are changes that occur during exercise in the extracellular fluid surrounding skeletal muscle cells. Such changes occur naturally as the cells consume more energy; in other words, the effect occurs automatically as a muscle exercises and only in the specific muscles working. The brain does not need to get involved in trying to adjust blood flow to the correct muscles. It happens automatically through this local mechanism.
One of these local chemical effects is an increase in extracellular K+.
QUESTION: Why do you suppose K+ tends increase around exercising muscle fibers? Answer
A second factor is an increased osmolarity in the extracellarly fluid.
QUESTION: Again, can you deduce why this occurs in exercising muscle? Answer
Two further local chemical changes with exercise are an increase in CO2 and an increase in H+ in the extracellular fluid. The reasons are pretty obvious.
OTHER ARTERIOLES: Most of the arterioles in the body are affected to at least some extent by local chemical factors that adjust the blood flow to the prevailing metabolic conditions. If any area has inadequate blood flow, the arterioles tend to dilate.
This effect can be quite pronounced if constriction of an artery causes a region be deprived of blood flow for a significant period (as when a blood pressure cuff is left inflated too long!). Once the contricting factor is removed, blood flow is greatly increased to the region for a while. This is termed reactive hyperemia and can be painful. This happens for example in Raynaud's disease.
One important local chemical factor affecting brain arterioles is the carbon dioxide level. If carbon dioxide levels fall, as with hyperventilation, the arterioles tend to vasoconstrict. The subsequent reduction in blood flow produces a feeling of lightheadedness.
The arterioles are absolutely a key effector organ in the control of mean arterial pressure. Recall our model for the arterial system, which is a two ended ballon. Pressure inside the balloon is determined by the amount of water in the balloon. First, this will change if there is a change in the flow of water into one end of the balloon. This represents the cardiac output.
Second, the amount of water in the balloon will change if there is a change in the rate at which water leaves the balloon. This is determined by the lumped effects of all the arterioles in the body and is termed the total peripheral resistance. Arterioles determine this because they are the smallest parts of the arterial system and thus provide most of the resistance to flow around the systemic circulation. Neither the capillaries, which are extremely numerous, nor the voluminous veins offer much resistance to the flow of blood.
As we move through different physiological situations, arterioles are constantly constricting and dilating. Without compensation, this would lead to changes in arterial pressure. The effectors functions that prevent this from happening are autonomic nerves affecting the cardiac output and the sympathetic nerves controlling arterioles in the skin, gut, inactive skeletal muscle and kidneys. Since usually there is a basal level of vasoconstriction caused by the sympathetic nerves, less sympathetic activity can cause vasodilation, while more sympathetic activity causes vasoconstriction.
Raynaud's phenomenon refers to the spasm of arterioles in the fingers or toes in response to cold and/or stress. In primary Raynaud's, the condition occurs on its own as a problem in the regulation of the arterioles. This is a common condition, and you will encounter people with it periodically. In secondary Raynaud's, some other disorder has the phenomenon as a symptom and usually occurs in the middle-aged or older. This is less common but the presence of some underlying serious disorder needs to be ruled out in someone with symptoms.
A typical patient with primary Raynaud's might be a young woman in a cool climate, such as Seattle. But it occurs commonly in men too and might show up at any age. Exposure to cold and/or stress causes a strong constriction of the finger or toe arterioles and the digits become white. But eventually painful reactive hyperemia causes flushing of the skin.
The basic treatments for Raynaud's are non-pharmacological. Keeping warm is especially important. Wearing mittens or gloves, and keeping the torso and head warm may make a big difference. If the initial cooling of the digits is prevented, there may be no cascading, strong vasoconstriction of the arterioles. Stopping smoking, reducing stress and exercise are likewise indicated.
Occasionally, however, pharmacological treatments become necessary. Calcium channel blockers are sometimes tried, as are alpha-blockers (since alpha adrenergic receptors mediate sympathetic vasoconstriction in skin). Pharmacological treatments are mainly used when Raynaud's is not primary, but secondary to some other disease process. Of course, if Raynaud's is secondary to some other disease, then treating that disease is an obvious approach.
Optional: The NIH has a good website at Raynaud's -- NIH.