The renin-angiotensin-aldosterone system is a complex of enzymes and hormones that maintain homeostasis. Regulates the balance of s alt and water in the body and the level of blood pressure.
Working mechanism
Physiology of the renin-angiotensin-aldosterone system originates at the border of the cortex and medulla of the kidney, where there are juxtaglomerular cells that produce peptidase (enzyme) - renin.
Renin is a hormone and the initial link of the RAAS.
Situations in which renin is released into the blood
There are several conditions in which the hormone enters the bloodstream:
- Decrease in blood flow in the kidney tissue - in inflammatory processes (glomerulonephritis, etc.), with diabetic nephropathy, kidney tumors.
- Decrease in circulating blood volume (with bleeding, repeated vomiting, diarrhea, burns).
- Fall in blood pressure. The arteries of the kidneys contain baroreceptors that respond to changes in systemic pressure.
- Change in the concentration of sodium ions. In the human body, there are accumulations of cells that respond to changes in the ionic composition of the blood by stimulating the production of renin. S alt is lost with profuse sweating, as well as vomiting.
- Stress, psycho-emotional stress. The juxtaglomerular apparatus of the kidney is innervated by sympathetic nerves, which are activated by negative psychological influences.
In the blood, renin meets with a protein - angiotensinogen, which is produced by liver cells and takes a fragment from it. Angiotensin I is formed, which is the source of action for the angiotensin-converting enzyme (ACE). The result is angiotensin II, which serves as the second link and is a powerful vasoconstrictor of the arterial system (constricts blood vessels).
Effects of angiotensin II
Goal: Increase blood pressure.
- Promotes the synthesis of aldosterone in the zona glomeruli of the adrenal cortex.
- Affects the center of hunger and thirst in the brain, causing a "s alty" appetite. Human behavior becomes motivated to seek water and s alty foods.
- Affects sympathetic nerves, promoting the release of norepinephrine, which is also a vasoconstrictor, but less weak in action.
- Affects blood vessels, causing them to spasm.
- Involved in the development of chronic heart failure: promotes proliferation, fibrosisvessels and myocardium.
- Decreases glomerular filtration rate.
- Slows down the production of bradykinin.
Aldosterone is the third component that acts on the terminal tubules of the kidneys and promotes the excretion of potassium and magnesium ions from the body and the reverse absorption (reabsorption) of sodium, chlorine, and water. Due to this, the volume of circulating fluid increases, blood pressure numbers rise, and renal blood flow increases. Aldosterone receptors are present not only in the kidneys, but also in the heart and blood vessels.
When the body reaches homeostasis, vasodilators (substances that dilate blood vessels) - bradykinin and kallidin - begin to be produced. And the RAAS components are destroyed in the liver.
Scheme of the renin-angiotensin-aldosterone system
Like any system, the RAAS can fail. The pathophysiology of the renin-angiotensin-aldosterone system manifests under the following conditions:
- Defeat of the adrenal cortex (infection, hemorrhage and trauma). A state of aldosterone deficiency develops, and the body begins to lose sodium, chloride and water, which leads to a decrease in the volume of circulating fluid and a decrease in blood pressure. The condition is compensated by the introduction of saline solutions and aldosterone receptor stimulants.
- A tumor of the adrenal cortex leads to an excess of aldosterone, which realizes its effects and increases blood pressure. The processes of cell division are also activated, there ismyocardial hypertrophy and fibrosis, and heart failure develops.
- Pathology of the liver, when the destruction of aldosterone is disturbed and its accumulation occurs. Pathology is treated with aldosterone receptor blockers.
- Renal artery stenosis.
- Inflammatory kidney disease.
The importance of RAAS for life and medicine
Renin-angiotensin-aldosterone system and its role in the body:
- takes an active part in maintaining a normal blood pressure;
- ensures the balance of water and s alts in the body;
- maintains the acid-base balance of the blood.
The system may malfunction. By acting on its components, you can fight hypertension. The mechanism of renal hypertension is also closely related to the RAAS.
Highly effective groups of drugs that are synthesized thanks to the study of RAAS
- "Prily". ACE inhibitors (blockers). Angiotensin I does not convert to angiotensin II. No vasoconstriction - no increase in blood pressure. Preparations: Amprilan, Enalapril, Captopril, etc. ACE inhibitors significantly improve the quality of life of diabetic patients, providing prevention of renal failure. The drugs are taken in the minimum dosage, which does not cause a decrease in pressure, but only improves local blood flow and glomerular filtration. Medicines are indispensable for kidney failure, chronic heart disease and serve as one of themeans of treating hypertension (if there are no contraindications).
- "Sartans". Angiotensin II receptor blockers. The vessels do not respond to it and do not contract. Drugs: Losartan, Eprosartan, etc.
The opposite of the renin-angiotensin-aldosterone system is the kinin system. Therefore, blocking the RAAS leads to an increase in the components of the kinin system (bradykinin, etc.) in the blood, which favorably affects the tissues of the heart and vascular walls. The myocardium does not experience starvation, because bradykinin enhances local blood flow, stimulates the production of natural vasodilators in the cells of the renal medulla and microcytes of the collecting ducts - prostaglandins E and I2. They neutralize the pressor action of angiotensin II. The vessels are not spasmodic, which ensures adequate blood supply to the organs and tissues of the body, the blood does not linger and the formation of atherosclerotic plaques and blood clots is reduced. Kinins have a beneficial effect on the kidneys, increase diuresis (daily urine output).
