RAAS Full Form

The renin–angiotensin–aldosterone system (RAAS) is a hormone system that controls blood pressure, fluid and electrolyte balance and systemic vascular resistance. When renal blood flow is diminished, the kidneys’ juxtaglomerular cells convert the precursor prorenin (which is already present in the blood) to renin and secrete it straight into the circulation. Plasma renin then converts angiotensinogen, which is produced by the liver, to angiotensin I, a decapeptide.  The angiotensin-converting enzyme (ACE) is present on the surface of vascular endothelial cells, primarily those in the lungs, and converts angiotensin I to angiotensin II (an octapeptide). Angiotensin II has a relatively short half-life of 1 to 2 minutes. Angiotensinases, which are found in red blood cells and vascular beds throughout the body, rapidly breakdown it into an angiotensin III heptapeptide.

Activation of RAAS

When there is a loss of blood volume or a drop in blood pressure, the system can be activated (such as in haemorrhage or dehydration). Baroreceptors in the carotid sinus interpret this drop of pressure. A reduction in the filtrate sodium chloride (NaCl) concentration or flow velocity can also activate it causing the macula densa to notify the juxtaglomerular cells to release renin.

• The juxtaglomerular apparatus (granular cells, modified pericytes in the glomerular capillary) releases the enzyme renin when the perfusion of the juxtaglomerular apparatus in the macula densa of the kidney declines.
• Angiotensin I is converted to an octapeptide, angiotensin II, by angiotensin-converting enzyme (ACE), which is located mostly in endothelial cells of capillaries throughout the body, the lungs, and kidney epithelial cells. In a 1992 study, ACE was discovered in all blood artery endothelial cells.
• The renin–angiotensin system’s main bioactive product, angiotensin II, binds to receptors on intraglomerular mesangial cells, causing them to contract along with the blood arteries around them and causing aldosterone to be released from the zona glomerulosa in the adrenal cortex. Angiotensin II is a hormone that has three functions: endocrine, autocrine/paracrine, and intracrine.

Cardiovascular effects of RAAS:

Through the vasa recta, angiotensin II reduces medullary blood flow. This reduces NaCl and urea washout in the kidney medullary compartment. As a result, greater NaCl and urea concentrations in the medulla aid tubular fluid absorption. Furthermore, greater fluid reabsorption into the medulla will boost sodium passive reabsorption through the Loop of Henle’s thick ascending limb. 

In addition to Na+ channels in the collecting ducts, angiotensin II activates Na+/H+ exchangers on the apical membranes (facing the tubular lumen) of cells in the proximal tubule and thick ascending limb of the loop of Henle. Increased salt reabsorption will result as a result of this.

Angiotensin II stimulates the secretion of aldosterone in the adrenal cortex. Aldosterone causes the tubules of the kidneys to reabsorb more sodium and water from the urine (e.g., the distal convoluted tubules and the cortical collecting ducts). As a result, blood volume increases and blood pressure rises. Potassium is secreted into tubules, becomes part of urine, and is expelled in exchange for sodium being reabsorbed into the circulation.

The Renin-Angiotensin System’s Importance:

The renin-angiotensin system regulates and maintains blood pressure in the cells of the body. This system reacts quickly to changes in a person’s blood pressure by releasing renin into the bloodstream.In the treatment of heart failure and hypertension, manipulative treatments are crucial. Reduces arterial blood pressure, blood volume, ventricular afterload, and ventricular preload, as well as vascular hypertrophy and reverse cardiac.

Conclusion:

The Renin-Angiotensin-Aldosterone System (RAAS) is a hormone system in the body that is responsible for blood pressure and fluid balance management. The three hormones renin, angiotensin II, and aldosterone make up the majority of the system. It is primarily governed by the rate of renal blood flow. The system will be described in this article, along with how it is regulated and certain clinically pertinent topics.

When renin is released into the bloodstream, it binds to angiotensinogen (a circulating layer) and causes it to be cleaved by proteolytic enzymes, yielding decapeptide angiotensin I. Angiotensin transforming enzyme, found in the vascular endothelium, separates two amino acids to produce angiotensin II (AII), which is also produced by various tissues in the body, including the brain and heart (AII).