The Kidneys' Role in Homeostasis

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The Kidneys' Role in Homeostasis by Mind Map: The Kidneys' Role in Homeostasis

1. Acid Base Balance

1.1. Decreased Body pH (more acidic)

1.1.1. Reabsorption of Bicarbonate happens mainly in the Proximal Convoluted Tubule (90%), and partially in the Distal Convoluted Tubule (10%) through a process called "Bicarbonate Trapping." The body uses carbonic anhydrase produced by the brush border of the convoluted tubules as a catalyst to break down Bicarbonate into CO2 and H2O. The CO2 is then diffused into tubular cells where it rejoins with H2O to form bicarbonate that is then released into the blood circulation.

1.1.2. Excess hydrogen ions are secreted into the proximal and distal tubules and excreted in urine to prevent the body from becoming too acidic, (pH too low) for example, after ingestion of a high protein meal

1.2. Increased Body pH (moer acidic)

1.2.1. Bicarbonate is freely filtered in the glomerulus and excreted in urine when plasma bicarbonate concentration is elevated, thus preventing from the body from becoming too basic (pH too high)

2. Blood Pressure

2.1. Changes in blood pressure are directly related to changes in blood volume which is controlled by a hormonal cascade known as the Renin- Angiotensin- Aldosterone- System, or RAAS. Cells located in the distal tubule called macula densa cells, along with renin-releasing cells in the arterioles of the glomerulus make up what's known as the juxtaglomerular apparatus (JGA). The JGA detects increases and decreases to the amount of blood flow to the glomerulus, or the GFR. Changes in blood pressure typically directly affect the GFR

2.1.1. Decreased Blood Pressure

2.1.1.1. Cells in the JGA sense a decrease in the GFR in the glomerulus and stimulate the renin-releasing cells to release renin, thus initiating the RAAS.

2.1.1.1.1. Renin stimulates the release of angiotensinogen which stimulates the release of angiotensin I which is activated by ACE and converted to angiotensin II. Angiotensin II causes vasoconstriction of the efferent arteriole of the glomerulus, increasing GFR, as well as peripheral vasoconstriction, raising systemic BP by decreasing the space within the blood vessels which exerts more pressure.

2.1.1.1.2. Angiotensin II also stimulates the release of aldosterone from the adrenal cortex. Aldosterone promotes the reabsorption of both sodium and water from the distal tubule, thus increasing blood volume and blood pressure. This is done by exchanging potassium or hydrogen for sodium

2.1.2. Increased Blood Pressure

2.1.2.1. Cells in the JGA sense increased GFR and send a negative feedback signal to the stop the release of renin, thus halting the RAAS system which leads to increased blood pressure. The excretion of sodium and water is permitted freely to decrease blood volume, and no vasoconstriction occurs.

3. Body Fluid Osmolarity

3.1. Antidiuretic Horomone (ADH) is directly influenced by blood osmolality.

3.1.1. Increased Blood Osmolarity

3.1.1.1. Osmoreceptors in the hypothalamus detect increased blood osmolality and relay a signal to the posterior pituitary gland to secrete more ADH. ADH then travels to the ADH receptors in the collecting ducts of nephrons and cause the water channels to open allowing more water to be reabsorbed out of the filtrate and into the blood stream to decrease blood osmolality.

3.1.2. Decerased Blood Osmolarity

3.1.2.1. Osmoreceptors in the hypothalamus detect decreased blood osmolarity and relay a signal to the posterior pituitary gland to stop secreting ADH. This is part of a negative feedback loop. The water channels in the collecting ducts remain closed and more water is excreted in the urine, increasing blood osmolality.

4. Body Fluid Volume

4.1. Extracellular fluid volume is largely influenced by sodium, the main extracellular ion. An increase in sodium will usually lead to an increase in body fluid volume and inversely, a decrease in sodium will usually lead to a decrease in body fluid volume. Body fluid volume and sodium levels are regulated by ADH and Aldosterone

4.1.1. Increased Body Water

4.1.1.1. Urine output is increased in order to prevent fluid overload in the body, for example, in the case of increased or excessive fluid ingestion. Less water is reabsorbed from the loop of henle into the medulla and water channels remain closed in the collecting duct. A less concentrated urine with lower specific gravity is produced since generally, the total amount of solutes excreted is less variable. The maximum urine output that can be produced is 23000mL

4.1.2. Decreased Body Water

4.1.2.1. Urine output is decreased when the body is lacking water, such as with decreased intake or excessive losses through vomiting, diarrhea, or sweating. ADH acts on the ADH receptors in the collecting ducts and water channels open allowing more water to be reabsorbed from the filtrate into the bloodstream. More water is also reabsorbed from the loop of Henle . A more concentrated urine with higher specific gravity is produced in order to still eliminate the required solutes and waste products. The least amount of urine that can be produced daily in order to still eliminate the necessary waste is approximately 300mL

5. Electrolyte Balance

5.1. Phosphate

5.1.1. Phosphate levels are linked to calcium levels. Phosphate and calcium are freely filtered at the glomerulus. Phosphate is a significant part of the buffering system which maintains the pH balance of the blood. Inorganic phosphate may exist as either an acid-phosphate (H2PO4-) or an alkaline phosphate (HPO4-)

5.1.1.1. Increased Serum Phosphate

5.1.1.1.1. When plasma phosphate levels rise above 1 mmol/L, some phosphate remains in the filtrate to be excreted in urine.

5.1.1.2. Decreased Serum Phosphate

5.1.1.2.1. When serum phosphate is below 1 mmol/L, all phosphate that enters the filtrate is reabsorbed in the proximal convoluted tubule.

5.2. Calcium

5.2.1. Calcium levels are related to both phosphate levels and magnesium levels.

5.2.1.1. Decreased Serum Calcium

5.2.1.1.1. Calcium-sensing cells in the parathyroid gland sense a decrease of plasma calcium and cause the release of PTH. PTH acts by stimulating reabsorption of calcium from bones and from the distal tubules of nephrons. As more calcium is conserved, more phosphate is lost in exchange.

5.2.1.2. Increased Serum Calcium

5.2.1.2.1. When calcium and calcitriol levels are elevated, a negative feedback loop is initiated, and PTH levels drop. The decrease in PTH allows calcium to be excreted in the urine and prevents the conversion of calcidiol to calcitriol.

5.3. Magnesium

5.3.1. Decreased Serum Magnesium

5.3.1.1. Magnesium balance is linked with calcium. PTH increases tubular reabsorption of magnesium in addition to calcium

5.4. Potassium

5.4.1. Potassium is the main intracellular ion. Only about 2% of the body's total potassium is extracellular. The only hormone that regulates potassium balance is Aldosterone. Aldosterone promotes the reabsorption of sodium and water from the nephrons and secretes potassium into the filtrate. Potassium has a reciprocal relationship with sodium. Potassium is also related with pH balance as potassium and hydrogen compete.

5.4.1.1. Decreased Extracellular Potassium

5.4.1.1.1. The kidneys are not as efficient at conserving potassium as they are at conserving sodium when there is a shortage. When K+ levels are normal or decreased, a negative feedback signal is sent to stop the secretion of aldosterone, thus preventing increased secretion of potassium.

5.4.1.2. Increased Extracellular Potassium

5.4.1.2.1. Increased K+ directly stimulates the release of aldosterone from the adrenal cortex which acts on the distal convoluted tubule of the nephron to trade either hydrogen or potassium for sodium in the distal tubule. In states of hyperkalemia potassium excretion will be prioritized over hydrogen.

5.5. Sodium

5.5.1. Sodium is the main extracellular ion. Sodium is directly related to body fluid volume, body fluid osmolality and blood pressure. Sodium will attract and "hold on" to water.

5.5.1.1. Decreased Extracellular Sodium

5.5.1.1.1. The kidney is able to conserve sodium quite well in the face of sodium shortage. Sodium deficit almost always goes with a fluid volume deficit. ADH and Aldosterone work to conserve sodium along with fluid and maintain blood pressure.

5.5.1.2. Increased Extracellular Sodium

5.5.1.2.1. Thus, the same systems which affect fluid volume excess and increased blood pressure will work to promote the excretion of excess sodium. First more water will be reabsorbed from the filtrate to correct osmolality balance via the ADH feedback loop. This will lead to increased fluid volume and blood pressure, stimulating the negative feedback loop of the RAAS which will prevent the secretion of renin and ultimately promote the excretion of both water and sodium. The body is able to eliminate up to 150mmol per day via the kidneys when sodium is in excess.