According to Bayer Health Care, the renin-angiotensin-aldosterone system becomes activated when the specialized cells of the distal tubules known as macula densa detect the decreased concentration of sodium and chloride ions. The reduction of NaCl concentration of the blood is a result of the presence of low blood pressure in the body. Once the decrease in blood pressure has been detected, the juxtaglomerular cells found in the kidneys will start discharging renin (an enzyme which breaks down proteins into shorter fragments). However, it is important to note that there are also other stimulus for the release of the proteolytic enzyme renin.
Klabunde added that the pathway will proceed once the renin in the blood starts breaking down the protein angiotensinogen. The breakdown of angiotensinogen would produce a shorter peptide with 10 amino acids called angiotensin I. Next, another enzyme called the angiotensin converting enzyme (ACE) would then act on angiotensin I to remove two of its amino acids to form another peptide called angiotensin II. Angiotensin II is important in the RAAS because it allows vasoconstriction which results to a rise in arterial pressure. It also stimulates the release of aldosterone by the adrenal cortex and vasopressin by the posterior pituitary. Aldosterone is responsible for the increased preservation of sodium and fluid in the body by the kidney and the increased elimination of potassium from the body. Similarly, vasopressin also contributes to the kidney’s increased retention of fluids by avoiding the elimination of fluids without the involvement of electrolytes like sodium and potassium. Lastly, the activation of the thirst centers found in the brain are also an important function of Angiotensin II.
Works Cited
Klabunde, R.E. Cardiovascular Physiology Concepts. Klabunde, 24 Apr 2014. Web. 20 Apr 2015.
Bayer Health Care. The renin-angiotensin-aldosterone system. Bayer Group, 2015. Web. 20 Apr 2015.
