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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 II exerts system wide effects, triggering aldosterone release from the adrenal cortex, direct vasoconstriction, and thirst behaviors originating in the hypothalamus. This is commonly known as the renin-angiotensin-aldosterone system.
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.
Proposed ACE catalytic mechanism. ACE is a central component of the renin–angiotensin system (RAS), which controls blood pressure by regulating the volume of fluids in the body. Schematic diagram of the renin–angiotensin–aldosterone system. Angiotensin II is a potent vasoconstrictor in a substrate concentration-dependent manner. [10]
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 ...
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 .
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).
The opposite mechanism is called transrepression. The hormone receptor without ligand binding interacts with heat shock proteins and prevents the transcription of targeted genes. Aldosterone and cortisol (a glucosteroid ) have similar affinity for the mineralocorticoid receptor; however, glucocorticoids circulate at roughly 100 times the level ...