Renin–angiotensin system in the context of "Circulatory system"

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⭐ Core Definition: Renin–angiotensin system

The renin–angiotensin system (RAS), or renin–angiotensin–aldosterone system (RAAS), is a hormone system that regulates blood pressure, fluid, and electrolyte balance, and systemic vascular resistance.

When renal blood flow is reduced, juxtaglomerular cells in the kidneys convert the precursor prorenin (already present in the blood) into renin and secrete it directly into the circulation. Plasma renin then carries out the conversion of angiotensinogen, released by the liver, to angiotensin I, which has no biological function on its own. Angiotensin I is subsequently converted to the active angiotensin II by the angiotensin-converting enzyme (ACE) found on the surface of vascular endothelial cells, predominantly those of the lungs. Angiotensin II has a short life of about 1 to 2 minutes. Then, it is rapidly degraded into angiotensin III by angiotensinases which are present in red blood cells and vascular beds in many tissues.

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Renin–angiotensin system in the context of Homeostasis

In biology, homeostasis (British also homoeostasis; /ˌhmiəˈstsɪs/ HOH-mee-ə-STAY-sis) is the state of steady internal physical and chemical conditions maintained by living systems. This is the condition of optimal functioning for the organism and includes many variables, such as body temperature and fluid balance, being kept within certain pre-set limits (homeostatic range). Other variables include the pH of extracellular fluid, the concentrations of sodium, potassium, and calcium ions, as well as the blood sugar level, and these need to be regulated despite changes in the environment, diet, or level of activity. Each of these variables is controlled by one or more regulators or homeostatic mechanisms, which together maintain life.

Homeostasis is brought about by a natural resistance to change when already in optimal conditions, and equilibrium is maintained by many regulatory mechanisms; it is thought to be the central motivation for all organic action. All homeostatic control mechanisms have at least three interdependent components for the variable being regulated: a receptor, a control center, and an effector. The receptor is the sensing component that monitors and responds to changes in the environment, either external or internal. Receptors include thermoreceptors and mechanoreceptors. Control centers include the respiratory center and the renin-angiotensin system. An effector is the target acted on, to bring about the change back to the normal state. At the cellular level, effectors include nuclear receptors that bring about changes in gene expression through up-regulation or down-regulation and act in negative feedback mechanisms. An example of this is in the control of bile acids in the liver.

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Renin–angiotensin system in the context of Juxtaglomerular cell

Juxtaglomerular cells (JG cells), also known as juxtaglomerular granular cells are cells in the kidney that synthesize, store, and secrete the enzyme renin. They are specialized smooth muscle cells in the tunica media of the walls of the afferent arterioles and - to a lesser extent - efferent arterioles of the glomerulus. They are located near the glomerulus, hence the name. In synthesizing renin, they play a critical role in the renin–angiotensin system and thus in autoregulation of the kidney.

Juxtaglomerular cells secrete renin in response to a drop in pressure detected by stretch receptors in the vascular walls, or when stimulated by macula densa cells. Macula densa cells are located in the distal convoluted tubule, and stimulate juxtaglomerular cells to release renin when they detect a drop in chloride concentration in tubular fluid. Together, juxtaglomerular cells, extraglomerular mesangial cells and macula densa cells comprise the juxtaglomerular apparatus.

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Renin–angiotensin system in the context of Prorenin

Prorenin (/prəˈrnɪn/) is a protein that constitutes a precursor for renin, the hormone that activates the renin–angiotensin system, which serves to raise blood pressure. Prorenin is converted into renin by the juxtaglomerular cells, which are specialised smooth muscle cells present mainly in the afferent, but also the efferent, arterioles of the glomerular capillary bed.

Prorenin is a relatively large molecule, weighing approximately 46 KDa.

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Renin–angiotensin system in the context of Renin

Renin (etymology and pronunciation), also known as an angiotensinogenase, is an aspartic protease protein and enzyme secreted by the kidneys that participates in the body's renin-angiotensin-aldosterone system (RAAS)—also known as the renin-angiotensin-aldosterone axis—that increases the volume of extracellular fluid (blood plasma, lymph, and interstitial fluid) and causes arterial vasoconstriction. Thus, it increases the body's mean arterial blood pressure.

Renin is not commonly referred to as a hormone, although it has a receptor, the (pro)renin receptor, also known as the renin receptor and prorenin receptor (see also below), as well as enzymatic activity with which it hydrolyzes angiotensinogen to angiotensin I.

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Renin–angiotensin system in the context of Angiotensinogen

Angiotensin is a peptide hormone that causes vasoconstriction and an increase in blood pressure. It is part of the renin–angiotensin system, which regulates blood pressure. Angiotensin also stimulates the release of aldosterone from the adrenal cortex to promote sodium retention by the kidneys.

An oligopeptide, angiotensin is a hormone and a dipsogen. It is derived from the precursor molecule angiotensinogen, a serum globulin produced in the liver. Angiotensin was isolated in the late 1930s (first named "angiotonin" or "hypertensin", later renamed "angiotensin" as a consensus by the 2 groups that independently discovered it) and subsequently characterized and synthesized by groups at the Cleveland Clinic and Ciba laboratories.

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Renin–angiotensin system in the context of Angiotensin-converting enzyme

Angiotensin-converting enzyme (EC 3.4.15.1), or ACE, is a central component of the renin–angiotensin system (RAS), which controls blood pressure by regulating the volume of fluids in the body. It converts the hormone angiotensin I to the active vasoconstrictor angiotensin II. Therefore, ACE indirectly increases blood pressure by causing blood vessels to constrict. ACE inhibitors are widely used as pharmaceutical drugs for treatment of cardiovascular diseases.

Other lesser known functions of ACE are degradation of bradykinin, substance P and amyloid beta-protein.

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