Biology » The Excretory System » Hormonal Control of Osmoregulatory Functions

Renin-Angiotensin-Aldosterone

Renin-Angiotensin-Aldosterone

The renin-angiotensin-aldosterone system, illustrated in the figure below proceeds through several steps to produce angiotensin II, which acts to stabilize blood pressure and volume. Renin (secreted by a part of the juxtaglomerular complex) is produced by the granular cells of the afferent and efferent arterioles. Thus, the kidneys control blood pressure and volume directly. Renin acts on angiotensinogen, which is made in the liver and converts it to angiotensin I. Angiotensin converting enzyme (ACE) converts angiotensin I to angiotensin II.

Angiotensin II raises blood pressure by constricting blood vessels. It also triggers the release of the mineralocorticoid aldosterone from the adrenal cortex, which 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 and decreases glomerular filtration rate. Medically, blood pressure can be controlled by drugs that inhibit ACE (called ACE inhibitors).

The renin-angiotensin-aldosterone pathway involves four hormones: renin, which is made in the kidney, angiotensin, which is made in the liver, aldosterone, which is made in the adrenal glands, and ADH, which is made in the hypothalamus and secreted by the posterior pituitary. The adrenal glands are located on top of the kidneys, and the hypothalamus and pituitary are in the brain. The pathway begins when renin converts angiotensin into angiotensin I. An enzyme called ACE then converts angiotensin I into angiotensin II. Angiotensin II has several direct effects. These include arterial constriction, which increases blood pressure, decreasing the glomerular filtration rate, which results in water retention, and increasing thirst. Angiotensin II also triggers the release of two other hormones, aldosterone and ADH. Aldosterone causes nephron distal tubules to reabsorb more sodium and water, which increases blood volume. ADH moderates the insertion of aquaporins into the nephridial collecting ducts. As a result, more water is reabsorbed by the blood. ADH also causes arteries to constrict. The hormone ANP is antagonistic to the angiotensin pathway. ANP decreases blood pressure and volume by increasing the glomerulus filtration rate, increasing reabsorption of sodium ions by the nephron, and by inhibiting the release of renin from the kidney and aldosterone from the adrenal gland.

The renin-angiotensin-aldosterone system increases blood pressure and volume. The hormone ANP has antagonistic effects. (credit: modification of work by Mikael Häggström)

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