The Bayliss effect maintains constant blood flow to organs such as the brain and kidneys despite everyday fluctuations in blood pressure. At elevated pressures, the effect induces vasoconstriction of vascular muscle. Disruption of the Bayliss effect results in persistent hyperemia and edema formation in the extracellular space.
What is the Bayliss effect?
The Bayliss effect keeps blood flow to organs such as the brain and kidneys constant despite day-to-day fluctuations in blood pressure. Blood pressure values are subject to fluctuations day after day. Despite these fluctuations, organ blood flow must be maintained at a constant level. The Bayliss effect contributes to the constant maintenance of organ perfusion. This myogenic autoregulation was first described by the British physiologist Bayliss and corresponds to a contraction response of the blood vessels that maintains the constancy of blood flow to organs and tissues as part of the local control in the circulation. The blood vessels are equipped with smooth muscle. When blood pressure changes, the vascular muscle cells respond to the new situation by either contracting or relaxing. The molecular cause of the Bayliss effect is thought to be the activation of mechano-sensitive receptors within the blood vessels. The Bayliss effect ultimately corresponds to a variant of circulatory regulation that is independent of the autonomic nervous system and its nerve fibers. While the effect can be demonstrated for the kidneys, gastrointestinal tract, and brain, the phenomenon does not appear to play a role for the skin and lungs.
Function and task
When blood flow increases within the small arteries or arterioles due to elevated blood pressure, vasoconstriction is thereby induced. Contraction of vascular smooth muscle is referred to as such, which in this case corresponds to a response to a pressure stimulus and can therefore be broadly described as a reflex. The mechanoreceptors in the vessels register the change in pressure and trigger vasoconstriction. This increases the resistance to flow in the affected vessels. The blood flow in the supply area of the vessels thus remains constant despite fluctuations in blood pressure. As soon as the mechanoreceptors in the vessels register lower blood pressure values again and thus register a decreasing supply of blood, vasodilation is initiated. The muscles of the vessels thus relax back to their basal tone. In this way, the Bayliss effect keeps blood flow to the kidneys, gastrointestinal tract, and brain largely constant and regulates values in these areas of the body relatively autonomously. The Bayliss effect shows efficiency at systolic blood pressure values of 100 to 200 mmHg. Molecular mechanisms underlie the effect. Arteries and arterioles with Bayliss effect carry mechano-sensitive cation channels in their walls. When these cation channels are opened, calcium ions flow into the muscle cells and form a complex with the protein calmodulin. Upon binding to form a complex, the enzyme myosin light chain kinase is activated. When phosphorylation occurs in the sense of interconversion of this kinase, the motor protein myosin II is activated with it. This motor protein enables the contraction of vascular smooth muscle cells. For any muscle contraction, the myosin and atkin filaments in the muscle must slide into each other. Myosin II is involved in this movement, as it is responsible for the binding site to the muscle’s atkin filament. The Bayliss effect is a type of circulatory regulation that operates independently of autonomic innervation of blood vessels. Thus, even if the vegetative connection is cut by severing the supplying nerves, the Bayliss effect remains intact. The mechanism can be blocked exclusively by the use of spasmolytic drugs such as papaverine, which induce vascular muscle cell relaxation.
Diseases and disorders
Disruption or even abolition of the Bayliss effect can have serious consequences for the organism. For example, permanent hyperemia of the organs in the affected supply area may result. Hyperemias are increased blood flow to a particular tissue or organ, as can result from dilation of the supplying blood vessels in the course of vasodilation. Hyperemias are usually the accompanying symptom of inflammation and are usually caused by locally released mediators.In addition, hyperemia is often associated with ischemia, which can cause a loss of muscle tone and a related decrease in wall tension in the vessels. Abrogation of the Bayliss effect may result in the spillover of fluid into individual organ structures because of the resulting hyperemia of a particular supply area. In this way, extracellular edema may develop. Edema is preceded by the leakage of fluid from the vessels, which eventually accumulates in the interstitial space. Edema formation is always preceded by a change in fluid movement between the interstitium and the capillaries. The laws of Starling’s equation play a major role in fluid leakage. In addition to the hydrostatic pressure of blood capillaries, the difference in oncotic vascular pressure between capillaries and interstitial space plays a role. The hydrostatic and oncotic pressures act against each other. While hydrostatic pressure causes water to leak into the interstitial space, oncotic pressure binds fluid within the capillaries. The two forces normally maintain near equilibrium. Edema can form only in the context of abnormal pressure values that are no longer in balance. Such abnormal pressure values occur, for example, with the failure of the Bayliss effect. Since the ion channel TRPC6 in particular is involved in the Bayliss effect, mutations of the gene coding for it, among others, can cause disturbances of the effect. Meanwhile, rare hereditary kidney diseases, for example, have been attributed to a mutation in the TRPM6 gene. Mutations can change the protein in the ion channel so much that it no longer functions. Magnesium deficiency and impaired calcium supply within the cells is the result.
