Self-regulating blood flow during changes in arterial pressure
The tendency of the blood flow to return to normal is called autoregulation. After active metabolism occurs, local blood flow in most tissues will be related to arterial pressure.
Mechanisms of “metabolism” and “biomechanics” are self-regulating mechanisms of muscle rather than from nerve stimulation.
In any tissue of the body, a rapid increase in arterial pressure causes an immediate increase in blood flow. However, within less than a minute, blood flow in most tissues returns to near normal, although arterial pressure remains elevated. The tendency of the blood flow to return to normal is called autoregulation. After active metabolism occurs, local blood flow in most tissues will be related to arterial pressure, as shown by the “acute” curve. Note that between arterial pressure 70 and 175 mmhg, blood flow only increased by 20-30% despite a 150 % increase in arterial pressure. In some tissues such as the brain and heart, self-regulation is even more stringent. For nearly a century, two theories have been put forward to explain this instantaneous adjustment: the metabolic theory and the biomechanical theory.
Figure. Effects of different arterial pressures on muscle blood flow. The red curve shows the effect when arterial pressure is increased for more than a few minutes. The blue dashed line shows the effect on blood flow when arterial pressure rises slowly over several weeks.
Metabolism is simply understood, the basic principles of blood flow regulation have been discussed in the previous section. therefore, when arterial pressure is raised too high, the excess blood flow delivers too much oxygen and other nutrients to the tissue and "dilute" the vasoconstrictors released by the tissue. These nutrients, especially oxygen, and the rise and fall of vasoconstrictor concentrations can cause vasoconstriction and a return to near-normal blood flow even though arterial pressure remains elevated.
However, biomechanics suggests another mechanism that is not related to metabolism to explain autoregulation. This theory is based on the observation of a sudden strain of small blood vessels when the smooth muscle of the vessel wall contracts. From this observation came the view that high arterial pressure would stretch blood vessels, causing vasospasm to react, the blood flow returning to near normal. In contrast, in a state of low blood pressure, the constriction is very little, leaving the smooth muscle to rest and, the pressure on the vessel wall is reduced and blood flow returns to normal.
The biomechanical response is inherent in smooth muscle, which can occur in the absence of hormonal or neurological influences. Mostly visible in arterioles, but also in arteries, small veins, and even lymph vessels. Contraction follows a biomechanical mechanism initiated by induced vasoconstriction depolarization, a rapid increase of Ca++ ions entering the cell from the intercellular space causing vasoconstriction. Changes in pulse pressure can also open or close ion channels affecting vasoconstriction. The exact mechanism by which pressure changes cause the opening or closing of the ion channels of the circuit is not yet elucidated but is most likely related to the mechanism by which pressure affects elements of the vessel wall or channels. circuit ions.
The biomechanical mechanism appears to be important in preventing excessive muscle contraction of blood vessels when blood pressure is increased. However, the role of this mechanism on vascular autoregulation remains unclear because the pressure-sensitive mechanism does not directly detect changes in tissue blood flow. Indeed, metabolic factors appear to be more plausible than biomechanics in certain circumstances where its metabolic demands are significantly increased, such as during muscle strength training, which can cause a paroxysmal increase in blood flow to skeletal muscle.