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Angiotensin, which is a protein, is a component of the renin-angiotensin-aldosterone system (RAAS), which performs important functions in the regulation of fluid balance and blood pressure in the human body. It has two forms: angiotensin I (AI) and angiotensin II (AG II). Generally, the function of angiotensin is to raise the blood pressure.
Formation of AI is brought about by the reactions between renin, produced by the kidneys, and angiotensinogen, produced by the liver. A specific enzyme produced in the lungs, called angiotensin-converting enzyme (ACE), then acts on AI, converting it to AG II. The first form, AI, does not commonly exert any functions in the body, while AG II has numerous effects.
AG II causes blood vessels to constrict, concentrating more blood flow to vital areas of the body. In the adrenal cortex, it stimulates the release of aldosterone, which makes the kidneys reabsorb more sodium and preserve water. The thirst center in the brain is also stimulated, thereby promoting an individual to drink more fluids. It also promotes the release of vasopressin, otherwise known as antidiuretic hormone, from the posterior pituitary gland. Vasopressin also increases retention of fluids by the kidneys and decreases urine volume.
Renin production in the kidneys is usually stimulated by low blood pressure or low blood volume, caused by factors such as inadequate intake of salt, bleeding, obstruction, or shock. Angiotensin II acts to make blood vessels in the kidneys and other organs constrict, limiting blood flow to these areas and diverting more blood flow towards the heart and the brain. Aldosterone and vasopressin mostly contribute in fluid retention and limiting urination. Sodium reabsorption in the kidneys increases, as sodium also aids in the retention of more fluids.
Atherosclerosis due to the accumulation of cholesterol in the blood often causes narrowing of the arteries. When arteries supplying the kidneys become narrowed and blood flow decreases, the kidney usually interpret this as low blood pressure, thereby activating the RAAS and eventually raising the blood pressure. Through this mechanism, renal hypertension develops.
Treatment of hypertension frequently includes the use of ACE inhibitors or angiotensin II receptor blockers (ARBs). ACE inhibitors mostly block the action of ACE on AI, thus preventing the formation of AG II. ARBs, on the other hand, block AG II from binding with receptors in the blood vessels, thus causing the arteries to dilate instead of constricting.
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