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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]
Sodium absorption by the distal tubule is mediated by the hormone aldosterone. Aldosterone increases sodium reabsorption. Sodium and chloride (salt) reabsorption is also mediated by a group of kinases called WNK kinases. There are 4 different WNK kinases, WNK1, WNK2, WNK3, and WNK4.
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 collecting duct system of the kidney consists of a series of tubules and ducts that physically connect nephrons to a minor calyx or directly to the renal pelvis.The collecting duct participates in electrolyte and fluid balance through reabsorption and excretion, processes regulated by the hormones aldosterone and vasopressin (antidiuretic hormone).
This illustration demonstrates the normal kidney physiology, including the Proximal Convoluted Tubule (PCT), Loop of Henle, and Distal Convoluted Tubule (DCT). It also includes illustrations showing where some types of diuretics act, and what they do. Renal physiology (Latin renes, "kidneys") is the study of the physiology of the kidney.
Antimineralocorticoid mechanism of action. Aldosterone is a mineralocorticoid which is synthesized in the adrenal glands. [5] When aldosterone is secreted from the adrenal glands, it binds to the mineralocorticoid receptor in the renal tubule cell and forms a complex. [6]
When renal blood flow is reduced (indicating hypotension) or there is a decrease in sodium or chloride ion concentration, the macula densa of the distal tubule releases prostaglandins (mainly PGI2 and PGE2) and nitric oxide, which cause the juxtaglomerular cells lining the afferent arterioles to release renin, activating the renin–angiotensin–aldosterone system, to increase blood pressure ...
Another mechanism proposed by RW Schrier [6] suggests that aldosterone involves synergistic processes. In addition to increasing renal perfusion pressure, the resultant volume expansion decreases proximal sodium reabsorption and increases sodium delivery to the distal nephron sites of mineralocorticoid action.