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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.
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 ...
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.
Hyperaldosteronism (the syndrome caused by elevated aldosterone) is commonly caused by either idiopathic adrenal hyperplasia or by an adrenal adenoma. The two main resulting problems: Hypertension and edema due to excessive Na+ and water retention. Accelerated excretion of potassium ions (K+). With extreme K+ loss there is muscle weakness and ...
In response to stress, the brain directly innervates the thyroid and pancreas for energy regulation, sends signals to the cardiovascular system to increase cardiac output, stimulates the adrenal glands to release cortisol and aldosterone, and releases hormones from the pituitary gland such as ACTH to regulate urine output through the renin ...
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).
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]
Kisspeptin directly increases release of aldosterone by several means, the first being through these receptors leading to a direct route to aldosterone release. [24] Secondly, the H295R adrenal cells stimulated by kisspeptin can synthesize aldosterone by breaking down pregnenolone more efficiently. [ 24 ]