Renal Regulation of Electrolytes: Potassium G30

The process of moving potassium from the blood into cells, primarily driven by the sodium-potassium pump.

A condition where potassium levels in the blood are abnormally high.

A condition where potassium levels in the blood are abnormally low.

The main organ responsible for regulating potassium levels in the body, by eliminating excess potassium.

The hormone that stimulates the sodium-potassium pump, causing potassium to move into cells.

The hormone that increases potassium uptake into cells, similar to insulin.

The main sites in the kidneys where potassium is regulated, either reabsorbed or secreted depending on the body's needs.

The movement of potassium from the blood into the urine.

A key player in potassium secretion, these cells located in the late distal and collecting tubules control the movement of potassium into the urine.

A major factor influencing potassium secretion. An increase in plasma potassium concentration stimulates the Na+/K+ pump, increasing potassium uptake by principal cells and ultimately leading to more potassium in the urine.

The main site of potassium regulation in the kidneys. This part of the nephron controls both reabsorption and secretion of potassium depending on the body's needs.

A crucial protein that pumps sodium out of the principal cells and potassium into them, contributing to the overall effect of aldosterone on potassium secretion.

This refers to the concentration difference of potassium between inside and outside the principal cell, influencing the movement of potassium across the cell membrane.

A protein channel in the cell membrane of principal cells that allows potassium to pass through, contributing to potassium secretion.

Potassium secretion in the kidney is increased by both increased fluid delivery and an increase in the number of 'high conduction back channels' in the tubular membranes.

High sodium intake decreases aldosterone secretion, which normally decreases potassium secretion. However, due to the increased fluid flow, potassium secretion is maintained.

Hypocalcemia causes increased nerve and muscle excitability, while hypercalcemia depresses neuromuscular excitability.

Only ionized calcium is biologically active, representing about 50% of the total calcium in the body. The remaining 50% is bound to plasma proteins or not ionized.

Alkalosis (high blood pH) causes increased plasma protein binding of calcium resulting in a lower level of ionized calcium, which can lead to hypocalcemia.

The majority of calcium in the body is stored in bones, with only a small fraction found in extracellular and intracellular fluids.

Parathyroid hormone (PTH) regulates bone uptake and release of calcium. It also stimulates vitamin D activation and increases renal tubular calcium reabsorption.

Calcium is not secreted by the kidneys. Therefore, excretion is dependent on how much is filtered and how much is reabsorbed.

The maximum amount of phosphate the kidneys can reabsorb per minute.

The process where the kidneys excrete excess phosphate when intake exceeds the transport maximum.

Parathyroid hormone (PTH) increases phosphate excretion by reducing reabsorption in the kidneys.

The process where the kidneys adjust their excretion rate of water and salt to match intake.

The pressure created by the blood pushing against the walls of the blood vessels.

The pressure created by the proteins in the blood pulling water back into the blood vessels.

A network of vessels that collect excess fluid from the interstitial spaces and return it to the bloodstream.

The process where the kidneys excrete more water and sodium in response to increased blood pressure.

Angiotensin II is a potent hormone that regulates sodium excretion. It decreases tubular sodium and water reabsorption, helping to control blood pressure.

The renin-angiotensin-aldosterone system (RAAS) plays a crucial role in regulating blood pressure and fluid balance. When blood pressure drops, the kidneys release renin, which triggers a cascade of events leading to the production of angiotensin II and aldosterone. These hormones increase sodium retention and vasoconstriction, ultimately raising blood pressure back to normal.

Aldosterone is a hormone produced by the adrenal glands that directly influences sodium reabsorption in the kidneys. It acts primarily on the collecting tubules and collecting ducts, increasing the reabsorption of sodium and water back into the bloodstream.

Atrial natriuretic peptide (ANP) is a hormone released by the heart in response to increased blood volume. It acts on the kidneys to promote sodium excretion, diuresis (increased urine production), and vasodilation, resulting in a decrease in blood pressure and volume.

An increase in blood volume can lead to a dangerous cascade of events. Congestive heart failure can cause reduced cardiac output and decreased blood pressure, triggering the RAAS pathway. This leads to sodium retention and fluid overload, worsening the heart's condition. If this positive feedback loop continues, circulatory congestion can develop.