Origin of blood pressure

The systolic arterial pressure is generated by the ejection capacity of the heart. The diastolic pressure corresponds to the continuous pressure in the arterial vascular system. The air vessel function and compliance of the large arteries limit the systolic value during ejection, so that the blood pressure in a healthy person cannot become too high.

Due to their buffer function, they also ensure a low blood flow during diastole. During physical exertion, the cardiac output and blood flow in the periphery must increase and the vascular resistance decreases. At the same time, the systolic arterial blood pressure rises more strongly than the diastolic value.

Arterial regulation of blood pressure

Since both too high and too low arterial pressure can damage the organism and individual organs, blood pressure must be regulated within certain ranges. However, it must also be possible to adjust and increase the arterial pressure in the case of changing loads. The basic prerequisite for this regulation is that the body can measure the blood pressure itself.

For this purpose there are so-called baroreceptors in the aorta, carotid artery and other large vessels. These measure the stretching of the arteries and pass the information on to the autonomic nervous system. The body can thus adapt to the given conditions.

For a more detailed explanation, a distinction is made between short-term, medium-term and long-term blood pressure regulation. The mechanisms of short-term regulation cause an adjustment of the arterial pressure within seconds. The most important mechanism is the baroreceptor reflex.

If a higher pressure is generated in the vascular system, the artery walls are stretched more. This is registered by the baroreceptors in the vascular walls and the information is transmitted to the sympathetic nervous system via the medulla oblongata in the spinal cord. The vessels are stretched and the volume of ejection from the heart is reduced, causing the pressure to decrease somewhat.

If, on the other hand, the pressure in the vessels is too low, the sympathetic nervous system reacts by narrowing the vessels and increasing the volume of blood ejected. The blood pressure increases. If the blood pressure is to be adjusted in the medium term, the renin- angiotensin- aldosterone system in particular reacts.

This consists of various hormones which are released in the kidneys and heart. If the body registers too little blood circulation in the kidneys, renin is released from the kidneys. This leads to the activation of angiotensin 2 and aldosterone and thus to a narrowing of the blood vessels.

The blood pressure rises. If the pressure in the kidneys is too high, renin secretion is inhibited and the aldosterone effect cannot take place. The blood pressure can also be regulated in the long term.

The kidney also plays an important role in this. If the arterial mean pressure increases too much, the volume in the vascular system and thus the pressure is reduced by increased excretion from the kidney (pressure diuresis). If the increased blood pressure puts too much strain on the atria, ANP is released from the heart.

This also causes increased fluid excretion from the kidneys. If the blood pressure drops too much, the neurohypophysis releases the antidiuretic hormone (ADH). This leads to increased water reabsorption from the collection tubes and distal tubules of the kidneys and thus to an increase in volume in the vascular system.

In addition, the ADH itself has a vasoconstrictive effect via special V1 receptors. The renin- angiotensin- aldosterone system is also effective in the long-term regulation, which, in addition to the vasoconstrictive effect, also causes an increased retention of water and sodium in the kidneys and thus in turn reduces the volume in the vascular system. Information about low blood pressure can be found here: low blood pressure