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24.18:

Autoregulation of Blood Flow

JoVE 핵심
Anatomy and Physiology
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JoVE 핵심 Anatomy and Physiology
Autoregulation of Blood Flow

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Autoregulation is the ability of tissues to maintain blood flow based on their metabolic requirements. It ensures optimal blood flow to support both mental and physical activities.

Autoregulation is mainly triggered by two types of stimuli — physical and chemical.

Physical stimuli, such as warm-up exercises, can lead to vasodilation, while body cooling can prompt vasoconstriction.

Additionally, the myogenic response of smooth muscle cells in the arteriole walls also helps autoregulation. When blood flow decreases, stretching of the arteriole walls decreases. This causes the smooth muscle cells to relax, leading to vasodilation and increased blood flow.

Various vasodilating and vasoconstricting chemicals can also trigger autoregulation.

Vasodilators, such as nitric oxide, lactate, and histamines, increase blood flow by relaxing smooth muscle cells in the arterioles.

In contrast, vasoconstrictors, such as serotonin, endothelin, and thromboxane A2, cause arteriole walls to contract, decreasing the blood flow.

24.18:

Autoregulation of Blood Flow

Autoregulation mechanisms are characterized by their inherent capacity for self-regulation without necessitating specific nervous stimulation or endocrine control. These mechanisms facilitate the adjustment of blood flow and, therefore, perfusion specific to each tissue region. This self-regulation encompasses chemical signals and myogenic controls.

Chemical Signaling in Autoregulation

Chemical signaling operates at the precapillary sphincter level, inciting either contraction or relaxation. Precapillary sphincters, when relaxed, allow blood to circulate into corresponding capillaries, whereas, during constriction, blood flow to the region is temporarily halted. Regulating factors of precapillary sphincters include:

  • • Nitric oxide (NO), a potent vasodilator, is discharged from endothelial cells, stimulating the relaxation of the sphincter under conditions of low oxygen, raised carbon dioxide, increased concentration of lactic acid or other cellular metabolism byproducts, elevated levels of potassium ions or hydrogen ions (decreasing pH), histamines, and heightened body temperature.
  • • Endothelins, potent vasoconstrictive peptides discharged by endothelial cells, elicit the contraction of the precapillary sphincter under opposite conditions. Constriction can also be induced by platelet secretions and certain prostaglandins.

These factors modify tissue perfusion through their effects on the precapillary sphincter mechanism that regulates blood flow to capillaries. Since blood is limited and not all capillaries can be filled simultaneously, blood flow is allocated based on tissue requirements and metabolic state, as indicated by these parameters. However, it is important to note that the primary control mechanism is the dilation and constriction of the arterioles supplying the capillary beds.

Myogenic Response in Autoregulation

The myogenic response is a reflexive reaction to the expansion of smooth muscle in the arteriole walls as alterations in blood flow occur through the vessel. This response primarily serves a protective role, guarding against significant variations in blood pressure and blood flow to preserve homeostasis. Insufficient perfusion (ischemia) leads to hypoxia, while excessive perfusion can inflict damage on smaller, delicate vessels of an organ. The myogenic response is a localized process aimed at stabilizing blood flow in the capillary network subsequent to the arteriole.

In conditions of low blood flow, the vessel's smooth muscle relaxes due to minimal stretching, facilitating dilation of the vessel and enhancing blood supply to the tissue. Conversely, when blood flow is excessive, the smooth muscle undergoes contraction in response to increased stretching, leading to vasoconstriction and a consequent reduction in blood flow.