Decreased kidney function causes chronic hypertension
Moderate increases in blood pressure also lead to a shortening of life expectancy. Severe hypertension means a 50% increase in mean blood pressure or above the normal range, and survival is not greater than a few years unless appropriate treatment is given.
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.
When a person has hypertension, this means that the mean arterial pressure is greater than the upper threshold of the accepted normal. A mean blood pressure reading greater than 110 mmHg (normally about 90 mmHg) is indicative of hypertension (this is the mean blood pressure that occurs when diastolic blood pressure is greater than 90 mmHg and systolic blood pressure is greater than 135). mmHg). A person with severe hypertension may have an average blood pressure increase of 150–170 mmHg, with diastolic pressure often as high as 130 mmHg and systolic pressure sometimes as high as 250 mmHg. Moderate increases in blood pressure also lead to a shortening of life expectancy. Severe hypertension means a mean blood pressure increase of 50% or above the normal range, and survival is not greater than a few years, unless appropriate treatment is given.
1. The overworked heart leads to premature heart failure and coronary heart disease, often fatal myocardial infarction.
2. The high pressure often destroys the main blood vessels of the brain causing the death of most of the brain, which appears as cerebral infarction. Clinically called the stroke. Depending on the part of the brain involved, it can cause death, paralysis, dementia, or other serious disorders.
3. High blood pressure always causes kidney damage, resulting in damage to many areas of the kidney, even kidney failure, haematuria, and death.
Increased hypertensive volume loading is important to understand the role of the kidney - the humoral mechanism in blood pressure regulation. Hypertensive volume overload means that blood pressure is caused by excessive accumulation of extracellular fluid in the body, some examples are as follows:
The volume-loaded hypertension experiment was induced by a decrease in renal mass and a concomitant increase in salt intake
The figure shows a typical experiment demonstrating hypervolemic hypertension in a group of dogs with 70% renal mass resection. At the 2nd circled point, the entire contralateral kidney was removed, leaving 30% of the renal mass. Note that this nephrectomy only increased blood pressure by an average of 6 mmHg. The dog was then given a saline solution instead of drinking water. Since a lot of salt doesn't quench thirst, the dog drank 2-4 times more than usual, and over the course of a few days on average his blood pressure rose 40 mmHg above normal. After 2 weeks the dog was given water instead of saline solution, blood pressure returned to normal in 2 days. At the end of the experiment the dog was again infused with saline and during this time the blood pressure rose rapidly and at a high level, again demonstrating hypervolemic hypertension.
Figure. Effect on arterial pressure of drinking 0.9% saline instead of water in dogs with 70% of renal tissue removed.
If we review the basic factors in the long-term regulation of blood pressure, it is easy to understand why hypertension occurs in the waste-volume experiment illustrated in Figure 18-9. First, a 70% reduction in kidney mass reduces the kidneys' ability to excrete salt and water. So salt and water accumulate in the body and a few days later blood pressure has risen enough to excrete excess salt and water.
Persistent changes in circulatory function in the progression of hypervolemic hypertension
The figure shows continuous changes. A week or so earlier than the “0” day point, kidney volume had decreased to only 30% of normal. Then at this point, the salt and water input increased sixfold and remained as if. The acute effect is an increase in extracellular fluid volume and cardiac output up to 20-40% of normal. Simultaneously, blood pressure begins to rise, but not in proportion to volume and cardiac output. The reason for the slow rise in blood pressure can be elucidated by studying the total peripheral resistance curve. This decrease is caused by a receptor mechanism, which temporarily weakens the rise in blood pressure. However, after 2-4 days the receptor adapts (reset), and is no longer able to prevent the rise in blood pressure. At this point, the blood pressure has risen to almost the highest level,
Figure. Progressive changes in important variables of the circulatory system during the first few weeks of volumetric hypertension. Of note is increased cardiac output initially as the underlying cause of hypertension. Autoregulation then returns cardiac output to near-normal while causing a secondary increase in total peripheral resistance.
After the grade changes in the circulation have taken place. Long-lasting secondary changes occurred over the next several weeks. Of particular importance is the gradual increase in total peripheral resistance, while cardiac output falls close to normal, mainly because of long-term autoregulatory mechanisms of blood flow. It is after cardiac output has risen to a high level and hypertension begins, excessive blood flow through the tissues increases constriction of the local arterioles.
Note that extracellular fluid volume and blood volume always return to near normal with a decrease in cardiac output. This results from two factors: first, an increase in arterial resistance reduces capillary blood pressure, which allows interstitial fluid to be reabsorbed into the bloodstream. Second, arterial hypertension causes the kidneys to excrete an excess fluid that initially accumulated in the body. Several weeks after volume loading, we found the following effects:
2. Significantly increased total peripheral resistance.
3. Extracellular fluid volume, blood volume, and cardiac output return to almost completely normal.
Thus, we can divide hypervolemic hypertension into two sequential phases. The first phase results from an increased fluid volume to increased cardiac output. This increase in cardiac output mediates hypertension. The second stage in hypervolemic hypertension is characterized by high blood pressure and high total peripheral resistance but the near-normal return of cardiac output that cannot be detected by conventional measurement techniques. Heart rate. Thus, the increase in total peripheral resistance in hypervolemic hypertension occurs after hypertension has developed and is, therefore, a consequence of hypertension rather than a cause of hypertension.
Hypervolemic hypertension in patients being maintained on haemodialysis
When a patient is maintained with an artificial kidney, it is especially important to keep the patient's fluid volume in the normal range by removing appropriate amounts of water and salt through each dialysis session. If this step is not taken and the extracellular fluid volume increases, hypertension almost always develops in the correct manner. That is, cardiac output increases first and causes an increase in blood pressure. The autoregulatory mechanism then returns cardiac output to normal while inducing a secondary increase in total peripheral resistance. Thus, in the end, hypertension presents as a type of peripherally resistant hypertension, even though the primary cause is excessive fluid accumulation.
Increased aldosterone causes high blood pressure
A type of hypervolemic hypertension that is caused by excess aldosterone in the body or, sometimes, by an excess of steroids. A small tumour in the adrenal gland sometimes secretes large amounts of aldosterone, a condition called “primary hyperaldosteronism.” Aldosterone increases the rate of salt and water reabsorption by the renal tubules, thereby reducing the loss of aldosterone. these substances are excreted in the urine while causing an increase in blood volume and extracellular fluid volume. Therefore, an increase in blood pressure occurs. If salt intake is increased simultaneously, the increase in blood pressure becomes more. if this condition persists for months or years, excessive arterial blood pressure often causes pathological changes in the kidneys that cause the kidneys to retain more salt and water plus a condition caused directly by aldosterone. , hypertension often eventually becomes fatal to the point of death.
Here again, in the early stages of this type of hypertension, cardiac output is increased, but in the later stages, cardiac output usually returns to near-normal while total peripheral resistance is secondarily elevated. .