VASODILATION: PHYSIOLOGY, VASODILATOR SUBSTANCES - ANATOMY AND PHYSIOLOGY - 2025

The vasodilation is a physiological process of expanding the transverse diameter of the arteries and arterioles in order to increase blood flow to a specific region of the body or, alternatively, lowering blood pressure.

The arteries are like "pipes" where blood flows 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 blood leaves the heart through the arteries and returns through the veins.

Dilated blood vessel

But unlike a conventional "pipe" such as that found in a house, arteries are very special, since they have the ability to modify their cross section (diameter) in response to different nervous, physical and chemical stimuli.

When the arteries decrease their transverse diameter (they shrink or become smaller) it is referred to as vasoconstriction, while the opposite phenomenon - that is, the enlargement of the cross section of the artery - is a vasodilation.

Depending on the stimulus that generates vasodilation, it can be local (of a particular arterial segment) or systemic (of all the arteries of the body).

Peripheral and cutaneous vasodilation

Aortic artery and its branches in anterior view

Peripheral vasodilation occurs when blood vessels that are located on 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 consequence of the release into the circulation of signaling molecules (prostacycins, nitric oxide).

It is a response to physiological changes in the body, such as infections (white blood cells can reach the infection earlier and kill the causative agents) or physical exercise (to cool down).

Cutaneous vasodilation refers to the increase in diameter of the blood vessels found in the skin, which causes an increase in blood flow. This effect also causes sweating and heat loss 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 the tissues).

When the oxygen concentration decreases in a given area - such as a leg, for example - a series of chemical mediators are generated that, by binding to the artery receptors that go to that hypoxic area, induce it to dilate, all this 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 is dilated is only the one that goes to that area. When hypoxia is generalized - for example, a person who rises from sea level to more than 3,000 meters above sea level - then vasodilation is generalized.

This is because chemical mediators and nerve signals are released throughout the body that induce vasodilation, as the 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, the ultimate goal of which is to produce vasodilation so that more white blood cells, antibodies and platelets reach the area. damaged.

When inflammation is generalized, as in 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 filtration pressure falls, a complex mechanism is triggered that induces vasodilation of the afferent arterioles (those that enter the glomerulus) and vasoconstriction of the efferent (exit) in order to increase the filtration pressure.

This is a local regulatory 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 the 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 pro-inflammatory cytokines. Among the effects of these substances is vasodilation.

By increasing the cross section of the arterioles in the area, the amount of blood that arrives also increases; Likewise, the amount of fluid 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 produces a local increase in temperature and redness, since the amount of blood in the area is higher than usual.

Once noxa ceases or pro-inflammatory substances are blocked with drugs, vasodilation ceases and, therefore, 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 vasodilation under physiological conditions is altitude sickness. When you go above a certain altitude (generally more than 2,500 meters above sea level) the amount of oxygen in your blood decreases; therefore, the body detects hypoxia and neurological and chemical signals are released that induce vasodilation.

Once this is installed the person begins to feel dizzy. This is because, due to vasodilation, blood pressure drops and 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, they may lose consciousness. All these symptoms are due to the effect of vasodilation on the central nervous system.

On the other hand, peripheral vasodilation causes fluids to escape more easily from the vascular space to the interstitial space (due to the enlargement 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 an increase in the volume of the hands and feet (peripheral edema), and accumulation of fluid in the lung (pulmonary edema) and in the brain (cerebral edema). If the vasodilation is not corrected, these changes can lead to death.

In pathological conditions

The previous example represents a typical physiological situation; however, under 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 body are the same.

Fortunately, situations that cause vasodilation 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 that vasodilation brings 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 capable of regulating their body temperature to keep it constant, and the capacity for capillary constriction / dilation has a lot to do with this.

At this point it can be said that the capillary network is largely responsible for the body's ability to maintain a stable temperature, since when the outside temperature drops, the arterial capillaries of the skin contract (vasodilation), thus reducing the radiation heat losses.

When the opposite happens -that is, that the ambient temperature rises-, then the cutaneous arterial capillaries dilate (vasodilation) and act as a radiator, allowing body heat to be eliminated.

It is clear that this phenomenon is very important in temperature control, but it is not the only physiological process in which it takes part.

Physiology

Describing in detail all the physiological processes where vasodilation takes part would require a full volume of a physiology book.

However, it is important to remember that vasodilation is essential for multiple processes such as digestion (vasodilation of the splanchnic bed during the digestive process), sexual arousal (erection in men, erectile tissue swelling in women) and the adaptation of the body 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 achieving lower blood pressure levels.

Vasodilator substances

There are many licit and illicit substances that can induce vasodilation. Substances that cause vasodilation include 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 propanolol), each of these capable of inducing vasodilation by different mechanisms.

At this point, special mention should be made of isosorbide dinitrate, whose powerful 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 due to several decades.

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