The vasodilation It is a physiological process that consists in the enlargement of the transverse diameter of the arteries and arterioles in order to increase the flow of blood to a certain region of the body or, failing that, lower blood pressure.
The arteries are like"pipes"through which blood circulates from the heart to the lungs (pulmonary arterial system). From these back to the heart through the pulmonary veins and from there to the rest of the body through the systemic arteries. It is a closed circuit where the blood leaves the heart through the arteries and returns through the veins.
Dilated blood vessel
But unlike a conventional"pipe"like the one that can be found in a house, the arteries are very special, since they have the capacity to modify their cross section (diameter) in response to different nervous, physical and chemical stimuli.
When the arteries decrease in their transverse diameter (shrink or become smaller), it is called vasoconstriction, whereas the opposite phenomenon - that is, the enlargement of the cross section of the artery - is a vasodilation.
According to the stimulus that the vasodilatation generates, it can be local (of a particular arterial segment) or systemic (of all the arteries of the body).
Index
- 1 Peripheral and cutaneous vasodilation
- 2 Stimuli that produce vasodilation
- 2.1 Hypoxia
- 2.2 Inflammation
- 2.3 Filtration pressure
- 3 Consequences of vasodilation
- 3.1 Clinical signs of local vasodilation
- 3.2 Clinical signs of systemic vasodilation
- 3.3 In pathological conditions
- 4 Vasodilation and thermoregulation
- 5 Physiology
- 6 Vasodilating substances
- 7 References
Peripheral and cutaneous vasodilation
Aortic artery and its branches in anterior view
Peripheral vasodilation occurs when blood vessels that are located in the periphery or extremities of the body increase in diameter. The cause is the relaxation of the smooth muscles in the walls of the vessels, as a result of the release of signaling molecules (prostacycins, nitric oxide) into the circulation.
It is a response to physiological changes in the body, such as infections (white blood cells can reach infection before and kill the causative agents) or physical exercise (to cool).
Cutaneous vasodilation refers to the increase in diameter of the blood vessels found in the skin, which causes an increase in the blood supply. This effect also causes sweating and loss of heat through the skin.
Stimuli that produce vasodilation
Hypoxia
The stimuli that can induce vasodilation are many, but of all these one of the most powerful is hypoxia (lack of oxygen in tissues).
When the concentration of oxygen decreases in a given area -such as, for example, a leg- a series of chemical mediators is generated that, joining the receptors of the artery that go to that area with hypoxia, induce it to dilate, all in order to get more blood to the area and, therefore, more oxygen.
If the hypoxia is localized as in the previous case, then the artery that dilates is only the one that goes to that area. When hypoxia is generalized - for example, a person who passes from sea level to more than 3000 meters high - then vasodilation is widespread.
This is due to the release of chemical mediators and nerve signals throughout the body that induce vasodilation, since tissues need oxygen.
Inflammation
Another factor that induces vasodilation is inflammation, and this can also be localized or generalized.
In cases of trauma, infection or injury, the white blood cells in the affected area produce a series of chemical mediators, whose ultimate goal is to produce vasodilation in order to reach more white blood cells, antibodies and platelets to the area. damaged
When inflammation is widespread, as in cases of sepsis, chemical mediators are everywhere inducing vasodilation.
Filtration pressure
Finally, there are pressure receptors at the level of the renal glomerulus that detect if the filtration pressure in the nephron is correct. When the low filtration pressure triggers a complex mechanism that induces vasodilatation of the afferent arterioles (those entering the glomerulus) and vasoconstriction of the efferent (exits) in order to increase the filtration pressure.
This is a local regulation mechanism whose objective is to keep the glomerular filtration pressure constant.
Consequences of vasodilation
The consequences of vasodilation vary depending on whether it is a local process or a systemic one.
The common denominator of both situations is that arteries, arterioles and arterial capillaries dilate; however, the clinical expression varies depending on the situation.
Clinical signs of local vasodilation
The classic example of local vasodilation is trauma. Shortly after the noxa (tissue damage) the area begins to swell; This is because white blood cells in the area release proinflammatory cytokines. Among the effects of these substances is vasodilation.
Increasing the cross section of arterioles in the area also increases the amount of blood that arrives; likewise, the amount of liquid that passes from the capillaries to the interstitial space increases, which manifests as swelling of the area.
On the other hand, the increase in blood flow causes local increase in temperature and redness, since the amount of blood in the area is higher than usual.
Once the noxa ceases or proinflammatory substances are blocked with drugs, vasodilatation ceases and, therefore, the clinical signs disappear.
Clinical signs of systemic vasodilation
When vasodilation occurs at a general level, the clinical signs are variable, depending largely on the intensity of the stimulus and the time of exposure.
The classic example of generalized vasodilatation under physiological conditions is altitude sickness. When passing a certain altitude (usually more than 2500 meters above sea level) the amount of oxygen in the blood decreases; therefore, the body detects hypoxia and chemical and neurological signals that induce vasodilation are released.
Once this is installed the person begins to feel dizzy. This is because, due to vasodilation, blood pressure drops and the perfusion pressure in the brain decreases.
Due to this drop in blood pressure it is also possible for the person to feel nauseous and, in the most severe cases, may lose consciousness. All these symptoms are due to the effect of vasodilation on the central nervous system.
On the other hand, peripheral vasodilatation causes fluids to escape more easily from the vascular space to the interstitial space (due to the increase in size of the capillary pores), which ultimately induces the accumulation of fluid in the extravascular space.
Due to this there is edema, which is manifested by increased volume of hands and feet (peripheral edema), and accumulation of fluid in the lung (pulmonary edema) and in the brain (cerebral edema). If vasodilation is not corrected, these changes can lead to death.
In pathological conditions
The previous example represents a physiological type situation; however, in pathological conditions the same changes occur, the classic example being septic shock. Under these conditions, the stimulus changes -which is no longer hypoxia but inflammation-, but the changes that occur in the organism are the same.
Fortunately, the situations that produce a vasodilatation as severe as the one described are not everyday, so it is not a situation that must be faced on a daily basis. In this sense, the benefits of vasodilatation to homeostasis are much greater than its deleterious effects in extreme conditions.
Vasodilation and thermoregulation
One of the main characteristics of homeothermic animals is that they are able to regulate their body temperature to keep it constant, and this has much to do with the ability to constrict / dilate the capillaries.
At this point it can be said that the capillary network is largely responsible for the ability of the body to maintain a stable temperature, since when the outside temperature drops, the arterial capillaries of the skin contract (vasodilation), thus decreasing the heat losses by radiation.
When the opposite happens -ie, that the ambient temperature rises-, then the cutaneous arterial capillaries dilate (vasodilatation) and act as a radiator, allowing to eliminate body heat.
It is clear that this phenomenon is very important in the control of temperature, but it is not the only physiological process in which it takes part.
Physiology
Describing in detail all physiological processes where vasodilation takes part would require a full volume of a physiology book.
However, it is important to remember that vasodilation is fundamental for multiple processes such as digestion (vasodilatation of the splanchnic bed during the digestive process), sexual arousal (erection in man, swelling of the erectile tissues in women) and adaptation of the organism to exercise, among other processes.
In addition, arterial vasodilation is essential to maintain stable blood pressure levels and within the normal range, to the point that many antihypertensive drugs are administered with the aim of inducing pharmacological vasodilation and thus achieve lower blood pressure levels.
Vasodilating substances
There are many licit and illicit substances that can induce vasodilation. Among the substances that produce vasodilatation are alcohol, opiate derivatives (such as morphine and heroin), as well as many medications.
Among the most important vasodilator drugs are calcium channel blockers (such as nifedipine and amlodipine) and beta-blockers (such as propranolol), each of which can induce vasodilation by different mechanisms.
At this point, special mention should be made of isosorbide dinitrate, whose potent vasodilator effect, especially at the level of the coronary bed, has allowed it to remain among the main drugs for the treatment of angina pectoris and acute myocardial infarction. several decades
References
- Moncada, S. R. M. J., Palmer, R. M. L., & Higgs, E. A. (1991). Nitric oxide: physiology, pathophysiology, and pharmacology. Pharmacological reviews , 43 (2), 109-142.
- Crawford, J. H., Isbell, T.S., Huang, Z., Shiva, S., Chacko, B.K., Schechter, A. N.,... & Ho, C. (2006). Hypoxia, red blood cells, and nitrite regulate NO-dependent hypoxic vasodilation. Blood , 107 (2), 566-574.
- Taylor, W. F., Johnson, J. M., O'Leary, D. O. N. A. L., & Park, M. K. (1984). Effect of high local temperature on reflex cutaneous vasodilation. Journal of Applied Physiology , 57 (1), 191-196.
- Imray, C., Wright, A., Subudhi, A., & Roach, R. (2010). Acute mountain sickness: pathophysiology, prevention, and treatment. Progress in cardiovascular diseases , 52 (6), 467-484.
- Lorente, J. A., Landin, L., Renes, E., De, R. P., Jorge, P. A. B. L. O., Rodena, E. L. E. N. A., & Liste, D. (1993). Role of nitric oxide in the hemodynamic changes of sepsis. Critical care medicine , twenty-one (5), 759-767.
- Landry, D.W., Levin, H.R., Gallant, E.M., Ashton, R.C., Seo, S., D'alessandro, D.,... & Oliver, J. A. (1997). Vasopressin deficiency contributes to the vasodilation of septic shock. Circulation , 95 (5), 1122-1125.
- López-Sendó, J., Swedberg, K., McMurray, J., Tamargo, J., Maggioni, A. P., Dargie, H.,... & Pedersen, C. T. (2004). Expert consensus document on β-adrenergic receptor blockers: The Task Force on Beta-Blockers of the European Society of Cardiology. European heart journal , 25 (15), 1341-1362.
- Cauvin, C., Loutzenhiser, R., & Breemen, C.V. (1983). Mechanisms of calcium antagonist-induced vasodilation. Annual review of pharmacology and toxicology , 2. 3 (1), 373-396.
- Joyner, M. J., & Dietz, N. M. (1997). Nitric oxide and vasodilation in human limbs. Journal of Applied Physiology , 83 (6), 1785-1796.
- Varu, V.N., Hogg, M.E., & Kibbe, M.R. (2010). Critical limb ischemia. Journal of vascular surgery , 51 (1), 230-241.
- Hirata, Y., Hayakawa, H., Suzuki, Y., Suzuki, E., Ikenouchi, H., Kohmoto, O.,... & Matsuo, H. (1995). Mechanisms of adrenomedullin-induced vasodilation in the rat kidney. Hypertension , 25 (4), 790-795.
- Charkoudian, N. (2003, May). Skin blood flow in adult human thermoregulation: how it works, when it does not, and why. In Mayo Clinic Proceedings (Vol. 78, No. 5, pp. 603-612). Elsevier
- Vatner, S. F., Patrick, T. A., Higgins, C. B., & Franklin, D. E. A. N. (1974). Regional circulatory adjustments to eating and digestion in conscious unrestrained primates. Journal of Applied Physiology , 36 (5), 524-529.
- Somjen, G., Fletcher, D.R., Shulkes, A., & Hardy, K. J. (1988). Effect of vaso-active intestinal polypeptide on systemic and splanchnic haemodynamics: role in vasodilation following mesenteric ischaemia. Digestion , 40 (3), 133-143.
- Adams, M. A., Banting, J. D., Maurice, D. H., Morales, A., & Heaton, J. P. W. (1997). Vascular control mechanisms in penile erection: phylogeny and the inevitability of multiple and overlapping systems. International journal of impotence research , 9 (2), 85.
- What is vasodilation? Taken from quora.com.