Cardiovascular physiology: Local control of blood flow
Tissues have some control over local blood flow via a number of key mechanisms:
Autoregulation of blood flow
Autoregulation refers to the ability of a tissue to regulate and maintain a constant blood flow despite variations in blood pressure.
The 2 mechanisms that contribute to autoregulation are:
Myogenic response
The myogenic response refers to arteriolar vasoconstriction in response to stretching of the vessel wall. It is thought that stretching opens calcium ion channels increasing entry of Ca2+. The increase in calcium ion levels triggers smooth muscle constriction resulting in vasoconstriction.
If blood flow into the arterioles is reduced the stretch activated Ca2+ channels remain closed allowing vasodilation to occur.
Carbon dioxide, potassium ions and adensoine are considered the most important factors and in some tissues hypoxia. These are considered further in the table below:
In inflammation vasodilation is mediated by the release of histamine and bradykinin.
When the clotting cascade is triggered serotonin and thromboxane A2 are released from activated platelets which promote vasoconstriction.
- Autoregulation
- Metabolic factors
- Local hormones (Autocoids)
Autoregulation of blood flow
Autoregulation refers to the ability of a tissue to regulate and maintain a constant blood flow despite variations in blood pressure.
Autoregulation occurs between pressures of 50 mmHg to 170mmHg
The 2 mechanisms that contribute to autoregulation are:
- Myogenic response
- Local vasodilatory factors
Myogenic response
The myogenic response refers to arteriolar vasoconstriction in response to stretching of the vessel wall. It is thought that stretching opens calcium ion channels increasing entry of Ca2+. The increase in calcium ion levels triggers smooth muscle constriction resulting in vasoconstriction.
If blood flow into the arterioles is reduced the stretch activated Ca2+ channels remain closed allowing vasodilation to occur.
Local vasodilatory factors
Certain local factors may promote vasodilation. With increased blood flow (hyperaemia) these factors become diluted which promotes vasoconstriction. When blood flow is reduced vasodilatory factors can accumulate and exert their vasodilatory effects.Metabolic factors
Metabolic hyperaemia or functional hyperaemia refers to increased blood flow to tissues when they are active. Hyperaemia is the result of vasodilatation caused by metabolites such as:- Carbon dioxide
- Potassium ions
- Adenosine
- Hydrogen ions
- Lactate
- Hypoxia
Carbon dioxide, potassium ions and adensoine are considered the most important factors and in some tissues hypoxia. These are considered further in the table below:
| Metabolite | Mechanism(s) of vasodilation |
|---|---|
| K+ | Stimulation of Na+-Ca2+ exchanger removing Ca2+ from the cell Hyperpolarising the cell |
| CO2 | Hypercapnia and resulting acidosis stimulate nitrous oxide Inhibition of Ca2+ entry into smooth muscle |
| Adensoine | Released as a breakdown product of ATP. Stimulates cAMP which causes vasodilation by reducing Ca2+ levels & inhibiting contractile kinase proteins in smooth muscle |
| Hypoxia | Reduced ATP causes ATP-sensitive K+ channels to open Increased potassium acts as described above |
In skeletal muscle the release of CO2, K+ and adensoine during exercise results in vasodilation of constricted capillaries. This is known as capillary recruitment.
Local hormones (Autocoids)
Autocoids act like local hormones and may stimulate a vasodilatory or vasoconstrictive response in situations such as inflammation or clotting.In inflammation vasodilation is mediated by the release of histamine and bradykinin.
When the clotting cascade is triggered serotonin and thromboxane A2 are released from activated platelets which promote vasoconstriction.