RAS Full-Form

The renin-angiotensin system (RAS) or the Angiotensin–aldosterone system (RAAS) controls blood pressure, the balance of fluids and electrolytes, and the resistance of the blood vessels in the body as a whole. When blood flow to the kidneys slows down, prorenin in the blood is changed into renin by juxtaglomerular cells. Renin is then released directly into the bloodstream. Angiotensin I, a decapeptide, is made from angiotensinogen, which was made by the liver. This is done by the plasma renin. The angiotensin-converting enzyme (ACE) on the surface of the vascular endothelial cells, especially those in the lungs, makes an octapeptide called angiotensin II. The half-life of Angiotensin II is between one and two minutes.

Renin-Angiotensin System

Adrenocortical stimulating and vasopressor activities are increased by angiotensin III, raising blood pressure and increasing aldosterone release from the adrenal cortex. Additionally, adrenocortical and vasopressor effects are seen by angiotensin IV.

As a powerful vasoconstrictor peptide, angiotensin II is one of the most commonly used medications to treat hypertension (high blood pressure). Angiotensin II also stimulates adrenal cortical aldosterone secretion. It is thought that aldosterone increases sodium reabsorption by the renal tubules, which causes water reabsorption and potassium excretion to occur (to maintain electrolyte balance)—extracellular fluid volume increases, which also raises blood pressure.

Blood pressure will be excessively high if the RAS is overactivated. ACE inhibitors, angiotensin II receptor blockers (ARBs), and renin inhibitors are all examples of medications that can improve blood pressure by disrupting different parts of the system. High blood pressure, heart failure, renal failure, and the adverse consequences of diabetes can all be managed using these prescription medications, which are commonly prescribed.

Activation

The mechanism can be activated in the event of a drop in blood volume or blood pressure (such as in haemorrhage or dehydration). Carotid sinus baroreceptors detect the drop in pressure and send a signal to the brain. The macula densa is activated, signalling the glomerular cells to release renin if the filtrate sodium chloride (NaCl) content or flow rate decreases.

Underutilized kidney cells (granular cells, modified pericytes in the renal capillary) release the enzyme, which is renin. Enzyme renin degrades the globular protein angiotensinogen into a decapeptide. One of the angiotensins is a decapeptide called angiotensin I.

Angiotensin-converting enzyme (ACE) changes angiotensin I into angiotensin II in the endothelial cells of capillaries all over the body, in the lungs, and in the epithelial cells of the kidneys. This happens in the lungs and in the capillaries of the kidneys. In a 1992 study, ACE was found in the endothelial cells of blood vessels.

By binding to receptors on these cells, angiotensin II, the main bioactive product of the renin-angiotensin system, causes intraglomerular mesangial cells to shrink and aldosterone to be released from the zona glomerulosa in the adrenal cortex. Angiotensin II has effects on the endocrine system, the autocrine/paracrine system, and the brain.

Local renin-angiotensin systems

Renin-angiotensin systems have been seen in places like the kidneys, adrenal medulla, heart, blood vessels, and nervous system. These systems are involved in a lot of different things, such as local cardiovascular regulation and functions that don’t have to do with the heart. Its precursor, prorenin, is found in many tissues, and more than half of the prorenin in the blood comes from places other than the kidneys. But, other than being a precursor to renin, it is still not clear what its role is in the body. Most of the time, renin comes from the blood outside of the kidneys, but some tissues may make it themselves. Angiotensinogen is taken from the blood or made locally in some tissues to make angiotensin I. This can be changed into angiotensin II with the help of enzymes like chymase, which is made locally by the angiotensin-converting enzyme  (ACE). This process can happen inside cells or between cells.

Paracrine regulation of aldosterone secretion in the adrenal glands, heart and vasculature, and the brain, where it is mainly independent of the circulatory RAS, is thought to represent a role of the RAS. The central and peripheral nervous systems can also use angiotensin to transmit sympathetic neurotransmission. The reproductive system, the skin, and the digestive system are examples of other organs that can represent oneself. Local systems may benefit or be harmed by medications aimed at the systemic system.

Fetal renin-angiotensin system

This mechanism is mostly sodium-depleting, as angiotensin II has little or no influence on aldosterone levels in the foetus. Angiotensin II levels in the fetus are substantially lower than in adults because of a lack of pulmonary blood flow, which prevents the ACE (which is found largely in the pulmonary circulation) from exerting its greatest effect.

Conclusion 

The renin-angiotensin system plays an important role when regulating arterial blood pressure and plasma sodium content. The renin-angiotensin system is turned on to maintain blood pressure in the vessels under control. This system rapidly releases renin into the bloodstream when blood pressure rises or falls. Suppression of the renin-angiotensin system is more effective for patients with renal and other cardiac diseases when treatment aims to stop the system completely. Angiotensin-Converting Enzyme I and Aliskiren, a recently authorised hypertension drug, can be taken together to create a dual blockage.