Local Control of Blood Flow

In this post we will be discussing the importance of arteriolar radius in the distribution of blood flow in the systemic circulation. I'll also explain the major mechanisms which regulate arteriolar radius.

Arteriolar Radius and the Distribution of Blood Flow

If you can remember from this post, you'll know that flow is determined by:

Flow = change in pressure / Resistance

Where the change in pressure is known as perfusion pressure.

All the organs in the systemic circulation are exposed to the same perfusion pressure, so the only way to alter blood flow to individual organs is to change the resistance. Arteriolar resistance is regulated intrinsically and extrinsically which allows the cardiac output between different organs to be changed according to need.

Intrinsic Regulation

The intrinsic regulation of blood flow dominates in critical tissues such as the brain, coronary circulation and working skeletal muscle.   

Active Hyperaemia

This is when blood flow is matched to metabolic rate and it is mediated by chemical changes in the tissue. As tissue metabolism increases, the concentration of vasodilators (CO2, K+ and other metabolic products) increases and the concentration of oxygen decreases. This results in vasodilation which reduces arteriolar resistance and increases blood flow. It also causes the reduction in the tone of precapillary sphincters which cause more capillaries to open. This decreases the diffusion distance and increases the total area of the capillaries. The increase in surface area, the increase in blood flow and the decrease in diffusion distance causes the amount of oxygen to increase and the vasodilators to be washed out of the tissue.

Reactive Hyperaemia: 

Reactive hyperaemia is the increase in blood flow in response to a period of inadequate blood flow. The chemical signals used are similar to what is used in active hyperaemia. During a period of reduced blood flow there is reduced O2 delivery and CO2 removal to and from cells. This causes extracellular O2 concentrations to decreases while the CO2 concentration increases, metabolites also build up. These conditions cause vasodilation which increases blood flow. The duration of reactive hyperaemia is directly proportional to the duration of vascular occlusion. 


Autoregulation:

This is the maintenance of blood flow despite changes in perfusion pressure. For example, between arterial pressures of about 70-170 mmHg blood flow increases by 30% although arterial pressure increases by 150%.  There are two possible mechainisms:

• Myogenic: an increase in perfusion pressure causes the arteriolar smooth muscle to stretch. The smooth muscle responds by contacting which increases resistance and decreases flow.
• Metabolic: An increase in blood pressure causes an increase in flow. This increases the amount of oxygen delivered to the tissues and causes the washout of vasodilators. This results in the contriction of the arterioles which increases resistance and decreases flow.  

Extrinsic Regulation

The parasympathetic nervous system has minimal influence on vascular smooth muscle, instead the sympathetic nerves play a major role. Sympathetic postganglionic neurons release noradrenaline which bind to α-adrenergic receptors on smooth muscle cells. This causes vasoconstriction.

There are 3 main hormones which are involved in the regulation of arteriolar radius:

• Adrenaline: this is released from cells in the adrenal medulla in response to sympathetic activity. In the skeletal muscle, β2 receptors respond to the adrenaline and cause vasodilation. In the GI (gastrointestinal) tract, α receptors respond to adrenaline by causing vasoconstriction.
• Antidiuretic hormone: this is synthesised in the hypothalamus and is secreted when hyperosmolaltiy and blood volume depletion occurs. The activation of V1 receptors causes arteriolar vasoconstriction and the activation of V2 receptors increases renal water reabsorption.
• Angiostensin II: Angiostensinogen is formed in the liver, this is converted to angiostensin I by renin. Angiostensis I is converted to angiostensin II by a converting enzyme present in endothelial cells. It has three major actions:

1. Renal Na+ (and hence water) retention. This is mediated by aldosterone
2. constriction of systemic arterioles
3. Regulation of glomerular filtration rate. 

So overall, extrinsic methods of regulation maintain stable arterial pressure, coordinating the circulatory system as a whole. Intrinsic mechanisms give individual organs the blood supply that it needs.
 
That's it for this post, see you next time :)