Aldosterone is one of the steroid hormones and is responsible for the body’s water and mineral balance. It retains increased water and sodium ions in the body, while potassium ions and hydrogen ions (protons) are excreted. Both aldosterone deficiency and aldosterone excess lead to severe adverse health effects.
What is aldosterone?
Aldosterone is a steroid hormone produced by the adrenal glands. It is also called the thirst or salt hormone because it is instrumental in controlling the body’s water and salt balance. The hormone represents a mineral corticoid, which belongs to the group of corticoid steroids. Its production takes place in the adrenal cortex along with other steroid hormones such as cortisol and sex hormones. Aldosterone is used to regulate blood pressure. If blood pressure falls, there is increased secretion of aldosterone. When blood pressure rises, aldosterone synthesis decreases. This regulatory mechanism is mediated by the renin-angiotensin-aldosterone system. Within the renin-angiotensin-aldosterone system, the mineral and water balance of the body is regulated depending on external influences. Thus, high water and salt loss reduces the excretion of urine by the kidneys while increasing thirst and salt hunger to restore balance. In this system, aldosterone plays a central role.
Anatomy and structure
Aldosterone, as mentioned earlier, represents a steroid hormone. Steroid hormones have the same basic chemical structure as cholesterol. Thus, cholesterol is also the parent molecule for the production of aldosterone and the other steroid hormones. Via the intermediate stage pregnenolone from cholesterol, pregesterone is formed by oxidation. After further hydroxylations of pregesterone and subsequent oxidations of the hydroxyl groups, aldosterone is finally formed. Its production takes place in the outer layer of the adrenal cortex, the zona glomerulosa. Its synthesis is triggered as a result of a decrease in blood volume as well as blood pressure or a too high potassium concentration (hyperkalemia) in the blood. Angiotensin II, which is formed as part of the renin-angiotensin-aldosterone system, acts as a mediator of synthesis. When the blood sodium concentration is increased, the biosynthesis of aldosterone is inhibited. This increases the concentration of atrial natriuretic peptide (ANP), thereby flushing out sodium by increasing urinary excretion. In turn, the regulating hormone ACTH stimulates the production of aldosterone.
Function and Tasks
Aldosterone functions to regulate the body’s water and mineral balance. It serves to maintain the physiological balance between potassium and sodium ions in the blood. The hormone causes increased incorporation of sodium channels (ENaC) and sodium transporters (Na+/K+-ATPase) into the plasma membrane of the epithelial cells of the kidney, lung and colon. These sodium channels are permeable to sodium ions, causing sodium to be reabsorbed from the primary urine or intestinal lumen. At the same time, the excretion of potassium and ammonium ions and protons increases. This results in an increase in extracellular volume, a decrease in potassium concentration, and an increase in blood Ph. Aldosterone is a hormone that can exert its activity via a corresponding receptor in the cell membrane. Certain aldosterone antagonists such as spironolactone or eplererone can inhibit the action of aldosterone by blocking the receptor. Cortisol also binds to the mineral corticoid receptor similarly to aldosterone. Therefore, it is oxidized to cortisone in the intestine, kidney or some other tissues. In this form, it can no longer bind to the receptor. It thus loses its antidiuretic efficacy, but separately from this function it continues to fulfill its tasks as a stress hormone. However, it no longer impedes the excretion of toxic substances in the urine. Aldosterone is regulated by the renin-angiotensin-aldosterone system. Within the framework of this system, a drop in blood pressure or a loss of water or sodium initially leads to the release of the enzyme renin from specialized parts of the kidney tissue. Renin in turn causes the formation of angiotensin II via the intermediate stage angiotensin I. Angiotensin II causes blood pressure to rise by constricting the fine blood vessels.At the same time, it stimulates the production of aldosterone, which induces the reabsorption of sodium and water.
Diseases
Both a deficiency and an excess of aldosterone can lead to significant health problems. In aldosterone deficiency, there is increased excretion of sodium and water. Symptoms include low blood pressure, fatigue, confusion, vomiting, diarrhea, and cardiac arrhythmias. The potassium level in the blood is too high. Newborns with aldosterone deficiency are referred to as salt wasting syndrome. In the first few days of life, they show weakness in drinking with refusal to eat, vomiting, diarrhea, dehydration and increasing apathy. The condition is life-threatening and must be treated immediately. There is both primary and secondary aldosterone deficiency. Primary aldosterone deficiency is due to disease of the adrenal glands. In extreme cases, so-called Addison’s disease can develop with total failure of the adrenal cortex. Here, in addition to aldosterone, the other steroid hormones are also missing. Secondary aldosterone deficiency, in turn, is due to a defective regulatory mechanism within the renin-angiotensin-aldosterone system. Treatment of aldosterone deficiency involves hormone replacement and treatment of the underlying disease. Overproduction of aldosterone can also have primary or secondary causes. Primary overproduction of aldosterone is usually caused by benign or, less commonly, malignant tumors in the adrenal glands. The primary form of overproduction is referred to as Conn syndrome, which manifests as muscle weakness, headache, thirst, and frequent urination. Secondary aldosterone overproduction shows similar symptoms and, as in secondary aldosterone deficiency, is caused by dysregulation in the renin-angiotensin-aldosterone system.
