true
TRUe
Aldosterone
Aldosterone
The major target of aldosterone is the distal tubule of the kidney, where it stimulates exchange of sodium and potassium. Three primary physiologic effects of aldosterone result:Increased resorption of sodium: sodium loss in urine is decreased under aldosterone stimulation.Increased resorption of water, with consequent expansion of extracellular fluid volume. This is an osmotic effect directly related to increased resorption of sodium.Increased renal excretion of potassium.Knowing these effects should quickly suggest the cellular mechanism of action this hormone. Aldosterone stimulates transcription of the gene encoding the sodium-potassium ATPase, leading to increased numbers of "sodium pumps" in the basolateral membranes of tubular epithelial cells. Aldosterone also stimulates expression of a sodium channel which facilitates uptake of sodium from the tubular lumen.
aldosterone; cortical collecting duct
potassium-sparing diuretics
The main region of aldosterone action is the distal convoluted tubule (DCT) and collecting duct of the kidneys. It functions to increase sodium reabsorption as well as enhance potassium excretion. The net effect of this is an increase in blood volume (via increased reabsorption of water), and thus an increase in blood pressure.
Sodium and potassium levels are controlled by secreting K+ and absorbing Na+. Sodium absorption by the distal tubule is mediated by the hormone aldosterone. Aldosterone increases sodium reabsorption.
Hyperkalemia. Captopril is an ACE (angiotensin converting enzyme) inhibitor which has various actions on the cardiovascular and renal systems. One of these actions in inhibition of the formation of Angiotensin II and aldosterone. Aldosterone acts to increase sodium (and water) reabsoprtion in the collecting duct of the nephron. In this process potassium is excreted. If aldosterone release is inhibited by Captopril then sodium reabsorption is decreased and potassium remains in the blood, leading to hyperkalemia.
Aldosterone is a hormone that increases the reabsorption of sodium ions and water and the release (secretion) of potassium ions in the distal convoluted tubules of the kidneys. This increases blood volume and, therefore, increases blood pressure. Drugs that interfere with the secretion or action of aldosterone are in use as antihypertensives.
involves aldosterone-induced secretion of potassium
The islets of Langerhans are clusters of cells found throughout the pancreas. These islets release various hormones, including insulin, glucagon, and somatostatin. Insulin's famous role is in the regulation of blood glucose concentration, but it also has a role in the regulation of sodium reabsorption and potassium secretion in the kidney.Insulin acts in special cells of the kidney called the principal cells of the collecting tubule. There it works in the same way as another hormone called aldosterone, which is released by the adrenal gland. Like aldosterone, insulin activates the sodium-potassium pump in the principal cell, ultimately increasing sodium reabsorption and potassium secretion. For this reason (and the fact that insulin also increases the shift of potassium into other cells of the body), insulin is commonly used to treat potassium overload (hyperkalemia).Now, I wouldn't go so far as to say that insulin controlssodium reabsorption and potassium secretion in the kidney, because that certainly isn't the case. Insulin can work to some degree in this regulation as described above, but the major mechanisms of sodium reabsorption and potassium secretion involve aldosterone, potassium concentration, and some other factors.This is the most obvious connection between the pancreas and kidney that I can think of. Perhaps there is something more relevant.
renin is created by the kidneys which in turn converts angiotensin 1 to angiotensin 2 this stimulates the formation of aldosterone to excrete urine. I would say that it increases the urine volume to decrease the plasma volume.