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Aldosterone stimulates Na + and water reabsorption from the gut, salivary and sweat glands in exchange for K +. Aldosterone stimulates secretion of H + via the H+/ATPase in the intercalated cells of the cortical collecting tubules; Aldosterone upregulates expression of NCC in the distal convoluted tubule chronically and its activity acutely. [18]
These cells then undergo a second migration from the dorsal aorta to form the adrenal medulla and other organs of the sympathetic nervous system. [44] Cells of the adrenal medulla are called chromaffin cells because they contain granules that stain with chromium salts, a characteristic not present in all sympathetic organs.
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).
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.
English: The renin–angiotensin system (RAS) or the renin–angiotensin–aldosterone system (RAAS). Start reading this schematic from the left, where it says "Decrease in renal perfusion (juxtaglomerular apparatus)".
The enzyme aldosterone synthase (also known as CYP11B2) acts in this location [3] [4] The expression of neuron-specific proteins in the zona glomerulosa cells of human adrenocortical tissues has been predicted and reported by several authors [5] [6] [7] and it was suggested that the expression of proteins like the neuronal cell adhesion ...
Aldosterone acts on the kidneys to provide active reabsorption of sodium and an associated passive reabsorption of water, as well as the active secretion of potassium in the principal cells of the cortical collecting tubule and active secretion of protons via proton ATPases in the lumenal membrane of the intercalated cells of the collecting tubule.
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.