There are many theories which try to explain the mechanism of auto-regulation of blood flow.
They are:
1. Myogenic theory
2. Tissue metabolite theory
3. Tissue fluid pressure theory
4. Renin-angiotensin theory, etc. (this theory is applicable only in kidneys)
1. Myogenic Theory (Fig. 3.53) According to This Theory:
i. When there is an increase in pressure, initially there will be an increase of blood flow.
ii. When blood flow increases, the smooth muscles present in the walls of the blood vessels get stretched.
iii. The stretching of the muscle will act as a stimulus (mechanical stimulus) to the muscle.
iv. The muscle starts responding to the stimulus by contracting.
v. Contraction results in the narrowing of the lumen diameter. Decreased lumen diameter increases the resistance to the flow (decrease in the radius of the lumen) and restricts the increase in the flow.
vi. Greater is the stretch; greater is the contraction of the smooth muscle fibers. Therefore, the total blood flow remains the same.
The role of myogenic theory in regulation of blood flow can be experimentally proved. When papavarine is injected, papavarine brings about the paralysis of smooth muscles.
Hence, after injection of papavarine, when the perfusion pressure is increased, there will be increase of blood flow without any autoregulation. It proves the role of smooth muscle fibers of blood vessels in the auto regulatory mechanism. This theory holds good for almost all organs.
2. Tissue Metabolite Theory:
i. At any given time, there will be some amount of metabolites in the tissues, e.g. the pCO2 in the tissues will be generally around 45 mm Hg.
ii. These metabolites exert vasodilator effect. Hence some amount of vasodilatation is maintained by these metabolites.
iii. When there is increase in perfusion pressure, to start with, there will be slight increase of blood flow.
iv. This brings about increased washout of metabolites from the tissues.
v. So the concentration of metabolites in the tissue is reduced.
vi. This reduces the vasodilator effect and leads to a little more vasoconstriction.
vii. Decreased lumen diameter will regulate the blood flow.
This theory holds good for all organs.
3. Tissue Fluid Pressure Theory:
i. There will be constant movement of fluids between blood and tissues at the level of capillaries.
ii. Exchange of fluid occurs at the level of capillaries because of the capillary dynamics.
iii. When there is increase of perfusion pressure, initially there will be increase of blood flow.
iv. This increases the hydrostatic pressure both at the arterial and venous end of capillaries.
v. Because of this, more fluid goes out at the arterial end of the capillary and less fluid returns at the venous end of the capillaries.
vi. This leads to increased accumulation of fluid in the tissue spaces.
vii. This in turn leads to compression of blood vessels.
viii. So blood flow is regulated.
This theory is applicable in the case of encapsulated organs, like kidney, liver, etc.
4. Renin-Angiotensin Theory:
i. When there is increase in perfusion pressure, there will be increase of blood flow to the kidney.
ii. This increases the filtration pressure in the nephrons.
iii. So the volume of filtrate is more in the nephrons.
iv. Because of this, more sodium will reach the distal convoluted tubules in the nephrons.
v. The amount of sodium reaching the distal convoluted tubules will be sensed by the macula densa of distal convoluted tubules.
vi. This leads to more renin getting released from juxtaglomerular cells.
vii. Renin acts on angiotensinogen present locally and brings about formation of angiotensin I.
viii. This angiotensin I is converted to angiotensin II (by converting enzyme present in the endothelial cell lining the blood vessels).
ix. Increased angiotensin II brings about the constriction of the arterioles (especially the afferent arteriole) in the kidneys.
x. This decreases the lumen diameter and the blood flow to the kidney is regulated.
This theory is applicable only to the kidneys.