Arterial blood pressure: controlled by pressure therapy

2021-05-26 02:08 PM

The amount of fluid in and out must be in perfect balance, this task is performed by nerve and endocrine control and by the control system in the kidney, which regulates salt and water excretion.

The sympathetic nervous system plays a major role in the immediate regulation of blood pressure, through the nervous system's influence on the total vascular resistance of the peripheral circulation, and the carrying capacity and pumping capacity of the heart.

However, there are also powerful mechanisms for regulating arterial blood pressure week to week and month to month. The long-term control of arterial blood pressure is inextricably linked with body fluid equilibrium, which is determined by the balance between fluid intake and output. For long-term survival, fluid intake and output must be perfectly balanced, a task performed by neuroendocrine and endocrine control and by the renal control system, which regulates salt excretion and secretion. country.

The figure shows the approximate effect of different arterial blood pressure levels on the urine output of an isolated kidney, demonstrating a significant increase in urine volume as blood pressure increases. This increased urine output is pressure diuresis. The curves in this figure are called the renal urine flow curve or renal function curve. In humans, when arterial blood pressure is 50 mm Hg, urine output is essentially zero. At 100 mm Hg it is normal, and at 200 mm Hg it is about six to eight times normal. Moreover, not only does the urine flow increase, the amount of sodium excreted is also almost equal, which is the phenomenon of hypernatremia.

Figure. A typical renal urine output curve is measured in an isolated perfused kidney, showing diuresis when arterial pressure is elevated above normal.

Experiments prove that the renal-fluid system controls arterial blood pressure

The figure shows the results of an experiment in dogs in which all neural reflex mechanisms for blood pressure control were blocked. Then, arterial blood pressure is suddenly raised by intravenous infusion of approximately 400 ml of blood. Note that cardiac output rapidly doubled to normal and mean arterial pressure rose to 205 mmHg, 115 mmHg greater than baseline. The middle curve is the effect of arterial hypertension on urine flow, which is increased 12-fold. With a large loss of urine fluid, both cardiac output and arterial blood pressure return to normal within the next hour. Therefore, the ability of the kidneys to remove excess water from the body is seen in response to hypertension and returning it to normal.

Figure. Increased cardiac output, urine output, and arterial pressure due to increased blood volume in dogs whose neural pressure control mechanisms have been blocked. This figure shows arterial pressure returning to normal after about an hour of fluid loss in the urine.

The renal-humoral mechanism provides a near-limitless counterregulatory benefit in the long-term regulation of arterial blood pressure

The figure shows a graphical method that can be used to analyse blood pressure regulation by the hydronephrosis system. This analysis is based on two separate curves that intersect: (1) the renal salt and water flow curves in response to increased blood pressure, the horizontal line representing water and salt intake.

For a long time, the water and salt out should be equal to the input. Furthermore, the only place on the graph in the figure where there is an equilibrium between inputs and outputs, where the two lines intersect, is called the equilibrium point. Now let's see what happens if the arterial blood pressure rises above or below the equilibrium point.

First, raise the arterial blood pressure to 150 mmHg. At this level, the amount of water and salt excreted increases 3 times. As a result, the body loses fluid, blood volume decreases, and arterial pressure decreases. Furthermore, this "negative balance" of the fluid will not cease until the blood pressure drops back to the same level. Indeed, even if the arterial blood pressure is only a few mmHg above the equilibrium threshold, the water and salt still lose a little more than the intake, so the blood pressure continues to fall until it is. return to equilibrium.

If the arterial blood pressure falls below the equilibrium point, the water and salt intake will be greater than the output. As a result, body fluid volume increases, blood volume increases, and arterial blood pressure return to equilibrium. Blood pressure always returns to the equilibrium point which is an almost infinite counter-regulatory principle to control blood pressure by the renal-humoral mechanism.

Figure. Analysis of arterial pressure regulation by equilibrating the renal output curve with the salt and water intake curves. The equilibrium point describes the level of arterial pressure to be corrected (a small fraction of the salt and water loss from the body via the non-adrenal glands is omitted in this section and similar figures).

Two major determinants of long-term blood pressure regulation

The figure shows two basic factors that determine the long-term blood pressure threshold.

As long as two curves are present (1) the renal salt and water flow, and (2) the salt and water intake remain exactly as shown in the figure, the final mean blood pressure value will be 100 mm Hg, which is the blood pressure threshold described by the equilibrium point in the figure. Furthermore, there are only two ways to alter this equilibrium. One way is to shift the blood pressure threshold of the curve (1), and the other is by changing curve (2). Therefore, two major determinants of the long-term arterial blood pressure threshold are as follows:

1. Degree of blood pressure variation of water and salt flow curves.

2.Water and the salt input threshold.

Figure. Two ways in which arterial pressure can be increased: A, by shifting the renal output curve to the right towards a higher-pressure level, or B, by increasing salt and water intake.

The functioning of these two determinants in blood pressure control. Several renal abnormalities shifted the curve by 50 mm Hg in the direction of hypertension (to the right). Note that the equilibrium has also moved to a higher than normal level of 50mmHg. Therefore, it can be said that if the renal flow curve shifts to a new blood pressure threshold, then the arterial blood pressure will change to this new level within a few days.

Figure B shows that a change in salt and water intake thresholds can also alter arterial blood pressure. In this case, the intake was quadrupled, and the equilibrium was shifted to a blood pressure level of 160 mm Hg, 60 mm Hg above normal. Conversely, reducing consumption will reduce arterial blood pressure.

Therefore, it is not possible to change the long-term mean arterial pressure to a new value without changing one or both of the underlying determinants of long-term arterial pressure or either - (1) salt and water intake or (2) the degree of change of the renal function curve along the pressure axis. However, if either change, one finds that the arterial blood pressure is then regulated to a new threshold, the arterial pressure at which the two new curves intersect.

However, in most people, the renal function curve is much steeper and changes in salt intake have only a modest effect on arterial blood pressure, discussed in the next section.

The chronic renal flow curve is much steeper than the acute curve

An important feature of pressure hypernatremia (and pressure diuresis) is that chronic changes in arterial blood pressure, lasting for days or months, have a much greater effect on the flow curve. salt and water compared with that observed for acute changes in blood pressure. So, when the kidneys are functioning normally, the salt-water flow curve is much steeper than the acute curve.

The strong effects of chronic hypertension on urine output appear because hypertension not only has a direct hemodynamic effect on the kidneys to increase excretion but is also indirectly influenced by neurological and Endocrine occurs when blood pressure rises. For example, high blood pressure reduces the activity of the sympathetic nervous system and certain hormones such as angiotensin II and aldosterone which tend to decrease the excretion of salt and water through the kidneys. Decreased activity of the antidiuretic system thereby amplifies the effects of pressure hypernatremia and pressure diuresis on increasing salt and water excretion in chronic hypertension.

In contrast, when blood pressure decreases, the sympathetic nervous system is activated and increases the formation of antidiuretic hormones, in addition to a direct effect on reducing the amount of salt and water excreted. The combination of the direct effects of blood pressure on the kidneys and indirect effects on the sympathetic nervous system and the endocrine system helps in the long-term regulation of arterial blood pressure and fluid volume.

The important neuroendocrine and endocrine effects of hypernatremia are particularly evident in chronic changes in sodium intake. If the kidneys and nervous and hormonal mechanisms are functioning normally, and with chronic increases in salt and water intake to six times normal, blood pressure will only increase slightly. Note that the blood pressure at equilibrium point B on the curve is roughly the same as at point A - the equilibrium point when salt intake is normal. In contrast, reducing salt and water consumption to less than one-sixth of normal generally had little effect on blood pressure. Therefore, many people are said to be salt insensitive because large variations in salt intake do not change blood pressure by more than a few mm Hg.

Individuals with kidney damage or excessive secretion of antidiuretic hormones, such as angiotensin II or aldosterone, may be salt-sensitive, with a renal flow curve similar to the acute curve. In these cases, even a moderate increase in salt intake can cause a significant increase in arterial blood pressure.

Figure. Output curves of acute and chronic kidney injury. Under steady-state conditions, the amount of salt and water by the kidneys is equal to the amount of salt and water. A and B represent equilibria for long-term regulation of arterial pressure when salt intake is normal or six times normal. Because of the steep chronic renal output curve, increased salt intake causes only small changes in arterial pressure. In individuals with impaired renal function, the slope of the renal output curve may decrease, similar to the acute curve, resulting in increased sensitivity of arterial pressure to changes in salt intake. to enter.

Several factors cause blood pressure to become salt-sensitive including loss of nephron function due to damage and excessive formation of antidiuretic hormones such as angiotensin II or aldosterone. For example, surgery to remove a large portion of the kidney or kidney damage from hypertension, diabetes, and kidney disease, all of which can make blood pressure more sensitive to changes in salt intake. In these cases, higher-than-normal blood pressure is needed to increase renal output enough to maintain a balance between salt and water intake and output.

There is evidence that long-term high salt use, lasting for many years, can damage the kidneys and eventually make blood pressure more sensitive to salt.