What is the aldosterone hormone? The function of aldosterone,
What is the aldosterone hormone?
The function of aldosteroneAldosterone (C 21 H 28 O 5) is a mineralocorticoid hormone compound that is secreted by the adrenal cortex. It is part of the Renin-Angiotensin-Aldosterone System, or RAAS, and is an integral part of the complex mechanisms that control the balance of water and electrolytes in the body. Its effect influences sodium, potassium, and water levels through the excretory and circulatory systems.
Function of aldosterone
The main function of aldosterone is to increase absorption in the last part of the distal tubule of the nephron and the collecting ducts. When directed to this point, the hormone binds to mineralocorticoid receptors on the membrane of the distal tubule. Once attached, the permeability of the distal tubular membrane increases. This facilitates the passage of potassium and sodium. Aldosterone also activates the hydrogen ion secretion mechanism in collectors. This regulates the pH value of the plasma and is therefore important for the acid-base balance. Aldosterone is also understood to play another role in the release of antidiuretic hormone (vasopressin or ADH) from the pituitary gland, causing the body to reabsorb more water through the nephron. However, aldosterone only affects about 3% of total water absorption. Therefore, it is considered a more suitable adjustment mechanism for small and regular changes in blood volume than a rescue measure in case of acute blood loss.
Aldosterone in the RAAS
The renin-angiotensin-aldosterone system, or RAAS, regulates blood pressure through a unique pathway made up of several hormones. These hormones (renin, angiotensin, and aldosterone) work together to produce the enzymes responsible for narrowing blood vessels and regulating secretion and excretion in the kidneys. The RAAS works in conjunction with the RAS or the renin and angiotensin system to quickly control blood pressure when needed.
Renin, or angiotensinogenase, is an enzyme and hormone that is produced by the kidney and released when the body’s fluid levels drop. Hypovolemia can be caused by dehydration, low water intake, persistent diarrhea or vomiting, blood loss, and systemic infections. The kidney needs a signal to release renin. This is administered through the autonomic nervous system, which response to signals sent by specialized baroreceptor cells in the walls of the heart and major arteries. There are two types of baroreceptors: high and low pressure. They recognize degrees of stretching of the arteries, veins, or myocardium. The first is located in the aortic arch and carotid artery. The latter in the pulmonary arteries, the largest veins, and the myocardium. When the baroreceptors notice a drop in blood volume, renin is released. Renin converts angiotensinogen into angiotensin I.
Angiotensinogen is a precursor protein and is made in the liver. In the presence of renin, angiotensinogen is converted to angiotensin I, another precursor. To make the final form, or angiotensin II, you need another enzyme made by the lungs called an angiotensin-converting enzyme or ACE. The term ACE may sound familiar because ACE inhibitors are popular drugs for controlling chronic high blood pressure. By inhibiting this enzyme, the blood vessels relax (see picture below) and blood pressure does not reach dangerous levels. An ACE is released, angiotensin I become angiotensin II.
Angiotensin II directly affects the walls of blood vessels, contracting them and thus raising blood pressure. It also ensures that blood is available to the most important organs, such as the heart, kidneys, and lungs. In the kidney, angiotensin II causes the arterioles that supply blood to each nephron to contract. The supplying or afferent arteriole contracts slightly; the efferent or outgoing arteriole contracts much more. This causes the blood between these vessels to back up, a vital mechanism, since, without continuous pressure, the exchange of ions, water, and other molecules cannot take place within the nephron.
In addition to its effect on the muscles of the blood vessels, angiotensin also increases the rate of sodium reabsorption within the nephron. Increasing sodium concentrations attract increasing water concentrations. By reabsorbing more sodium into the blood, the nephrons automatically reabsorb more water, increasing blood volume.
Angiotensin II also indicates the release of aldosterone from the adrenal cortex. Aldosterone increases the volume of water reabsorbed into the circulatory system by allowing even greater reabsorption of sodium. In addition, both aldosterone and angiotensin II signal the release of antidiuretic hormone (ADH or vasopressin) from the posterior pituitary gland. As one of its names suggests, ADH is a vasopressor or vasoconstrictor. It also increases the reabsorption of water in the nephron as shown below.
Aldosterone vs. ADH
While both aldosterone and the antidiuretic hormone are hormones that are secreted to increase the volume of water in the body and both act on the distal tortuous tubules and collecting tubules of the nephron, their similarities end here.
ADH is a fast-acting, lipophobic peptide hormone. Aldosterone is a slightly slower-acting (but longer-lasting) lipophilic steroid hormone, more precisely a corticosteroid hormone.
Aldosterone is synthesized and released by the adrenal glands; The prohormone form of ADH is produced in the hypothalamus but released by the pituitary gland. Aldosterone also affects the movement of sodium molecules across the nephron tubule membrane by increasing their permeability, while ADH makes these membranes more permeable to water. This means that aldosterone increases osmotic pressure and ADH allows water molecules to respond to this change.
When blood pressure rises, high-pressure receptors send signals to the brain that slow the heart rate and widen the blood vessels. If you experience hypovolaemia or a sudden leakage of fluid from the circulatory system, such as B. In syncope episodes, the low-pressure receptors in the pulmonary arteries, large veins, and the atrial and ventricular walls cause the opposite. They send signals to the brain, causing an increased heart rate and narrowing of the blood vessels. Both reactions are called baroreflex. Depending on the position of the baroreceptors, the signals travel along the nerves and end in the medulla oblongata.
To lower blood pressure, the brainstem activates the parasympathetic nerves to reduce cardiac output. This happens through a slower heart rate and less pronounced heart muscle contractions. At the same time, the medulla oblongata sends inhibitory signals to the sympathetic nerves, which relax the walls of the blood vessels and cause vasodilation. This dilation means more room for the same amount of blood, resulting in lower blood pressure.
To raise blood pressure, the medulla activates sympathetic nerves that increase the heart rate and the force of heart muscle contractions, increasing cardiac output. The parasympathetic nerves are inhibited, as a result of which the relaxing effect on the vessel walls is canceled and the vessels narrow. This pushes more blood into a smaller space within the circulatory system and increases the pressure in the blood vessels.
The role of adrenoceptors in raising and lowering blood pressure.
Other mechanisms are also involved when baroreceptors signal hypovolemia. These have a greater effect than RAAS and take effect when the pressure drops or rises well beyond the normal range. Below are the steps that lead to hemorrhagic shock, for example, in the case of severe blood loss. Note how low blood volumes lead to kidney failure due to the inability to maintain pressure on the glomerulus, ending any leakage.
Adrenaline is released from another region of the adrenal glands (the medulla) along with the neurotransmitter noradrenaline. These create alpha and beta effects to raise blood pressure. Both alpha and beta-adrenoceptors are made up of two groups: 1 and 2. Agonists of alpha-1 adrenoceptors bind to alpha-1 receptors in peripheral blood vessels, causing your muscles to contract and blood to the organs and most redirect critical systems. An agonist is a product that triggers a chemical reaction when it comes into contact with a receptor. Alpha-2 adrenergic receptor agonists bind to alpha-2 receptors and inhibit the release of noradrenaline (noradrenaline). Hence, it has the opposite effect of the Alpha-1 function. Beta-1 adrenergic receptor agonists act on the myocardium, creating additional tachycardia and contractility, but also act to release renin, thereby initiating the RAAS cycle. Beta-2 adrenergic receptors dilate the blood vessels and airways of critical organs to increase the supply of oxygen. The beta-2-way also increases glucose production and allows the skeletal muscles to contract with much more force.
The adrenal glands are located above the kidneys and are also called the adrenal glands. They produce a variety of endocrine hormones that act as chemical messengers within the confines of the body. Aldosterone is produced in the zona glomerulosa of the adrenal cortex, which lies just below the surface. The production of aldosterone requires an enzyme called aldosterone synthase. Congenital deficiencies in aldosterone synthase and other enzymes necessary for aldosterone production lead to hyponatremia and hyperkalemia. This shows that aldosterone primarily maintains the correct levels of sodium and potassium in the body.
Another ingredient in aldosterone is cholesterol. It is important that the hormones are lipid-based so that they can easily and quickly penetrate the phospholipid membranes of the recipient cells. The interaction of cholesterol with various enzymes can produce numerous steroid hormones. Depending on their function, steroid hormones or corticosteroids are divided into mineralocorticoids (aldosterone), glucocorticoids (cortisol), and sex corticosteroids (estrogen, progesterone, and androgen). The image clearly shows the range of chemicals produced by the adrenal gland and where. In the upper right, a small box shows the position of the adrenal gland in the kidney.
What is a mineralocorticoid?
Aldosterone is a mineralocorticoid, which means that its effects are involved in maintaining mineral levels. When activated, aldosterone binds to specific mineralocorticoid response elements (ERM), where it can increase the reabsorption of ions and water back to the body and bypass the excretory system. This leads to increased extracellular fluids, higher blood pressure, and lower levels of potassium in the body. Since aldosterone is only responsible for small amounts of water, its contribution to extremely high or low blood pressure values is minimal for a short time, but its constant long-term effect on the balance of mineral salt and water is decisive. This critical role can be seen in the symptoms of people with adrenal disease.
Overproduction of aldosterone by the adrenal gland is classified as either primary or secondary. Primary aldosteronism in both adrenal glands is due to bilateral adrenal hyperplasia or Conn’s syndrome (an adrenal tumor) and is rare. Unilateral primary adrenal hyperplasia and the familial inherited form are even rarer.
Secondary hyperaldosteronism is more common than the primary form, but it does not yet affect a significant percentage of the world’s population. It is caused by hyperactivity of the RAAS system, which is often the result of edema, renin-producing tumors, ascites, and renal artery stenosis, leading to poor blood flow to the kidney even with normal blood volumes.
The symptoms of primary hyperaldosteronism (or primary aldosteronism) are minor but can progress to hypertension, hypokalemia, and hypomagnesemia. The secondary symptoms of hyperaldosteronism spread similarly from asymptomatic to elevated blood pressure and lower potassium levels. The more general symptoms that are often mistaken for other diseases include fatigue, headache, polyuria, polydipsia, and metabolic alkalosis. The blood plasma renin-aldosterone ratio (ARR) test is used to distinguish primary from secondary hyperaldosteronism.
Hypokalemia is the result of increased sodium reabsorption in the nephron, an effect caused by the hormone aldosterone, which increases the volume of water in the body. When sodium is absorbed, potassium is excreted. Magnesium levels can be low because the body’s electrolyte balance is also often dependent. Low potassium levels are often accompanied by low calcium and magnesium levels.
Hypoaldosteronism is an equally rare condition that occurs due to an aldosterone deficiency. This deficiency is classified as hyporeninemic or hyperreninemic hypoaldosteronism, the accompanying blood renin levels. A small number of those affected are mostly kidney, diabetic or seriously ill patients. Other risk factors include lead poisoning and heart medications.
Long-term hyperkalemia as a result of hypoaldosteronism has a direct effect on the muscles, as potassium is required for muscle contraction. The symptoms of low aldosterone are therefore palpitations, muscle weakness, and irregular heartbeat. Others include nausea and difficult-to-control fluctuations in blood pressure.
Medicines for blood pressure
Medicines for high blood pressure are divided into different classes. The general functioning of the following classes has been discussed at some point in this article because blood pressure medication works in one or more of the same regions as RAAS.
Angiotensin-converting enzyme inhibitors suppress angiotensin levels, a major component of RAAS. Lower angiotensin levels mean less vasoconstriction. ACE inhibitors are teratogenic; This means that a pregnant woman’s fetus who takes this drug will also experience low blood pressure, as well as hyperkalemia and kidney failure.
By reducing the cardiac output, the blood pressure is lowered. Beta-blockers reduce the heart rate and the force of the heart muscle to contract. Beta-blockers are known to cause extremely slow heartbeats (bradycardia) of about 30 beats per minute and patients must be carefully monitored.
Angiotensin II receptor blockers
Angiotensin II receptor blockers (ARBs) also have a very similar effect on RAAS as the group of ACE inhibitors. The difference between an ACE inhibitor and an ARB is that the former limits the main component of angiotensin II production, which stops the conversion of angiotensin I to II, while the latter prevents the end product from binding to the receptors of the blood vessels. The effect of these two groups is essentially the same. However, the longevity of ACE inhibitors and the reluctance of drug companies to replace them creates a huge debate over which of the two is the best option.
When blood pressure is high due to hypervolemia, usually due to obesity, stress, electrolyte imbalances, low physical activity, chronic alcohol consumption, heart disease, and kidney problems, diuretics can clear the excess fluid through sodium excretion. To do this and avoid certain side effects, certain groups work on different levels. This is shown in the picture below, where the actions of the three main groups are shown in different parts of the nephron.
The three main groups are thiazide diuretics, potassium-sparing diuretics, and loop diuretics. Thiazide diuretics inhibit sodium and chloride ion reabsorption early in the nephron (in the proximal segment of the distal convoluted tubule), but later, and in part due to the influence of aldosterone on ion cotransporter proteins that allow passage of salts through the tubular membrane, this effect is somewhat offset. This compensation is insufficient to cancel the sodium-lowering effect of the proximal segment but results in low potassium levels.
Potassium-sparing diuretics, the second group, were developed in response to hypokalemia that has occurred in patients prescribed thiazide diuretics. These drugs mainly affect the balance between sodium and chloride. More sodium (and more water) is added to the ultrafiltrate and potassium remains. Therefore, these drugs have the potential to cause hyperkalemia.
The last group is made up of loop diuretics. These act very early along the nephron, at the end of the loop of Henlé (hence the name) and in front of the proximal convoluted tubule. This type of diuretic binds to cotransporter proteins to slow or stop the reabsorption of sodium and chloride ions. This is very similar to the mechanism of thiazides, but the early onset of action along the tubule means that the loop diuretics are much stronger. Consequently, thiazides are used to treat high blood pressure in people with relatively good kidney function; Loop diuretics are most effective in patients with poor kidney function and low filtration rates.
By central or local action, through the vasomotor center of the medulla oblongata or directly on the smooth muscles of the blood vessels, vasodilators enlarge the lumen of the vessel, creating more space for blood circulation and reducing blood pressure. Vasodilators are not the main therapy for hypertension, but they are used in combination with other antihypertensive drugs. Because they also increase blood flow to the heart, vasodilators are used primarily in cardiac patients.
Combined alpha and beta-blockers
Dual alpha and beta receptor blockers or alpha-beta adrenergic blockers have a dual role. As alpha-blockers, they relax the smooth muscles of the blood vessels. As beta-blockers, they slow the heart rate and decrease the force of the heart muscle contraction. This dual mechanism can lead to dizziness when standing up abruptly or syncope when blood pressure is too low.
What is the aldosterone hormone? The function of aldosterone