The vasomotor center (VMC) is a portion of the medulla oblongata in the brainstem, that, together with the cardiovascular center and respiratory center, regulates blood pressure and other homeostatic processes. Vasomotor center is a fairly archaic term since this function relies not on a single brain structure (“center”) but rather represents a presympathetic network of interacting neurons.
Upon increase in carbon dioxide level at central chemoreceptors, it stimulates the sympathetic system to constrict vessels. This is opposite to carbon dioxide in tissues causing vasodilatation, especially in the brain. Cranial nerves IX (Glossopharyngeal nerve) and X Vagus nerve both feed into the vasomotor centre and are themselves involved in the regulation of blood pressure.
The peripheral circulation is extremely important for transporting blood around the body, exchange of nutrients with tissues and storing blood. As the tissues in the body vary their need for blood e.g. during exercise, the peripheral circulation will match the flow to the demand. In this article, we will look at how flow is regulated through the peripheral circulation.
Oxygenated blood leaves the left side of the heart via the aorta. This is a large elastic artery. The aorta progressively branches into smaller muscular arteries and thereafter into arterioles and metarterioles, finally ending in capillaries, which provide the blood supply at a tissue level. The pressure drops as we move from the aorta to the capillaries. The aorta has minimal resistance to flow, as compared to the arterioles, which have much higher resistance.
By regulating the vasomotor tone of arterioles (amount of tension/contraction of the smooth muscle in the walls), we can control the blood flow to the capillary beds. This is achieved by controlling the vasoconstriction and vasodilation of the arterioles.
At rest, there is a high vasomotor tone i.e. the tonic contraction of the smooth muscle is higher. This is because the tissues require less blood during rest. The sympathetic nervous system is largely responsible for controlling the vasomotor tone. This causes noradrenaline release, which then acts on ?1 GPCRs (G-protein coupled receptors).
The vasomotor tone of arterioles can be altered in response to changes in tissue requirements for blood flow.
Metabolically active tissues release vasodilator metabolites such as H+, CO2, K+, adenosine and lactate. These have a knock on effect in reducing the vasomotor tone by causing vasodilation of the arterioles through smooth muscle relaxation. As the resistance in the arteriole has reduced, the blood flow to the tissue can increase. This is useful as it allows the blood to transport metabolites away from the tissue, thus helping to limit potential toxic effects to the tissue. Once the metabolites have been removed, the vasomotor tone will return back to its normal level.
Myogenic factors can also alter vasomotor tone. For example, when the arterioles experience a rapid increase in intraluminal pressure such as due to violent coughing, the arteriolar smooth muscle will contract in order to defend itself from the rise in pressure.
Additionally, the arteriolar endothelium can release biological factors known as autocoids. These behave in a similar way to hormones and can therefore increase or decrease the vasomotor tone.