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Aldosterone release causes sodium and water retention, which causes increased blood volume, and a subsequent increase in blood pressure, which is sensed by the baroreceptors. [39] To maintain normal homeostasis these receptors also detect low blood pressure or low blood volume, causing aldosterone to be released.
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 .
Aldosterone synthase is a protein which is only expressed in the zona glomerulosa [5] of the adrenal cortex and is primarily regulated by the renin–angiotensin system. [6] It is the sole enzyme capable of synthesizing aldosterone in humans and plays an important role in electrolyte balance and blood pressure. [7]
In the adrenal cortex, angiotensin II acts to cause the release of aldosterone. Aldosterone acts on the tubules (e.g., the distal convoluted tubules and the cortical collecting ducts) in the kidneys, causing them to reabsorb more sodium and water from the urine. This increases blood volume and, therefore, increases blood pressure.
The outermost layer, the zona glomerulosa is the main site for the production of aldosterone, a mineralocorticoid. The synthesis and secretion of aldosterone are mainly regulated by the renin–angiotensin–aldosterone system. The zona glomerulosa cells express a specific enzyme aldosterone synthase (also known as CYP11B2).
Schematic diagram of the renin–angiotensin–aldosterone system. Angiotensin II is a potent vasoconstrictor in a substrate concentration-dependent manner. [10] Angiotensin II binds to the type 1 angiotensin II receptor (AT1), which sets off a number of actions that result in vasoconstriction and therefore increased blood pressure.
ACTH then travels to the adrenal glands and induces the release of cortisol into the bloodstream. [7] In Cushing's syndrome, this process occurs in excess. Some symptoms of an individual with Cushing's syndrome include low tissue protein levels, due to muscle and bone atrophy, and high blood glucose levels. Sodium levels also see an increase ...
This causes the release of aldosterone into the blood. Aldosterone acts primarily on the distal convoluted tubules and collecting ducts of the kidneys, stimulating the excretion of potassium ions into the urine. [65] It does so, however, by activating the basolateral Na + /K + pumps of the tubular epithelial cells. These sodium/potassium ...