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The renin-angiotensin-aldosterone system (RAAS) stabilizes blood pressure and volume via the kidneys, liver, and adrenal cortex.
Describe hormonal control by the renin-angiotensin-aldosterone system
Renin, a hormone produced by the juxtaglomerular apparatus in the kidneys, converts angiotensinogen (which is made in the liver) to angiotensin I.
Angiotensin I is then converted to angiotensin II by the angiotensin converting enzyme (ACE), increasing blood pressure by causing vasoconstriction of the blood vessels.
Angiotensin II causes the release of aldosterone which is produced by the adrenal cortex; it functions to maintain both sodium and water levels (osmotic balance) in the blood.
Angiotensin II also causes the release of antidiuretic hormone (ADH) which functions to conserve water in the body when volume is low; it does this by inserting aquaporins in the collecting duct of the nephron to promote water reabsorption.
The atrial natriuretic peptide (ANP) is another hormone that is produced to function as a vasodilator and lower blood pressure by preventing sodium reabsorption.
The renin-angiotensin-aldosterone system (RAAS) is a hormone system that regulates blood pressure and water (fluid) balance . This system proceeds through several steps to produce angiotensin II, which acts to stabilize blood pressure and volume. Renin is secreted by a part of the juxtaglomerular complex and produced by the granular cells of the afferent and efferent arterioles. Renin is a circulating enzyme that acts on angiotensinogen, which is made in the liver, converting it to angiotensin I. Defective renin production can cause a continued decrease in blood pressure and cardiac output. After renin facilitates the production of angiotensis I, angiotensin converting enzyme (ACE) then converts angiotensin I to angiotensin II. Angiotensin II raises blood pressure by constricting blood vessels and also triggers the release of the mineralocorticoid aldosterone from the adrenal cortex. This, in turn, stimulates the renal tubules to reabsorb more sodium. Angiotensin II also triggers the release of anti-diuretic hormone (ADH) from the hypothalamus, leading to water retention in the kidneys. It acts directly on the nephrons, decreasing glomerular filtration rate. Thus, via the RAAS, the kidneys control blood pressure and volume directly. Medically, blood pressure can be controlled by drugs that inhibit ACE (called ACE inhibitors).
Mineralocorticoids are hormones synthesized by the adrenal cortex that affect osmotic balance. One type of mineralocorticoid, known as aldosterone, regulates sodium levels in the blood. Almost all of the sodium in the blood is reclaimed by the renal tubules under the influence of aldosterone. As sodium is always reabsorbed by active transport and water follows sodium to maintain osmotic balance, aldosterone manages not only sodium levels, but also the water levels in body fluids. Aldosterone also stimulates potassium secretion concurrently with sodium reabsorption. By contrast, absence of aldosterone means that no sodium is reabsorbed in the renal tubules; all of it is excreted in the urine. In addition, the daily dietary potassium load is not secreted; retention of potassium ions (K+) can cause a dangerous increase in plasma K+ concentration. Patients who have Addison's disease have a failing adrenal cortex and cannot produce aldosterone. They constantly lose sodium in their urine; if the supply is not replenished, the consequences can be fatal.
Antidiuretic hormone or ADH (also called vasopressin) helps the body conserve water when body fluid volume, especially that of blood, is low. It is formed by the hypothalamus, but is stored and released from the posterior pituitary gland. It acts by inserting aquaporins in the collecting ducts, promoting reabsorption of water. ADH also acts as a vasoconstrictor (constricting blood vessels) and increases blood pressure during hemorrhaging.
Atrial Natriuretic Peptide Hormone
The atrial natriuretic peptide (ANP) hormone lowers blood pressure by acting as a vasodilator (dilating or widening blood vessels). It is released by cells in the atrium of the heart in response to high blood pressure and in patients with sleep apnea. ANP affects salt release; because water passively follows salt to maintain osmotic balance, it also has a diuretic effect. ANP also prevents sodium reabsorption by the renal tubules, decreasing water reabsorption (thus acting as a diuretic) and lowering blood pressure. Its actions suppress the actions of aldosterone, ADH, and renin.
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