Renal Regulation of Potassium, Calcium, Phosphate & Magnesium PDF

This is the renal regulation of potassium, calcium, phosphate and magnesium. Uh, this is still module one. Uh, the last chapter got in chapter 30. Normally, potassium levels are around 4.2 MQ per liter, seldom rising or falling more than 0.3 huge. Only about 15 dynamics are in the Zaire fluid, wher...

This is the renal regulation of potassium, calcium, phosphate and magnesium. Uh, this is still module one. Uh, the last chapter got in chapter 30. Normally, potassium levels are around 4.2 MQ per liter, seldom rising or falling more than 0.3 huge. Only about 15 dynamics are in the Zaire fluid, whereas a single meal as intake can be as high as 50 MQ, meaning failure to rapidly adjust potassium concentration in the extracellular fluid quickly can cause hyperkalemia and even cardiac arrest. 98% of total body potassium is intracellular. Redistribution of potassium between intracellular and extracellular compartments provides a first line defense against changes in extracellular potassium concentration. The intracellular compartment can serve as an overflow during hyperkalemia and as a source of potassium during hypokalemia. Maintenance of the balance between intake and output of potassium depends primarily on, uh, renal excretion, uh, as only 5 to 10% is excreted in the feces. After ingestion, most of the potassium rapidly moves into the cells until it can be eliminated by the kidneys. Insulin stimulates the sodium potassium ATP pump, causing potassium movement into the cell, and ostrum increases potassium uptake as well as stimulation of beta adrenergic receptors, meaning those treated for hypertension with beta blockers tend to have hyperkalemia. Strenuous exercise can cause hyperkalemia due to skeletal muscle leakage. Renal excretion is determined by the rate of potassium filtration. The rate of potassium reabsorption by the tubules and the rate of potassium secretion by two. Normally, 756 MQ are filtered by the glomerular capillaries each day. The rate of filtration is relatively constant due to other regulatory mechanisms for GFR. Rate of reabsorption in the proximal tubule, and then the loop of hennelly is constant. So the most important sites for regulation of potassium excretion are the late distal tubules and the cortical collecting tubules that these segments can reabsorb or secrete, depending on the needs of the body and those with high protein diets. The rate of excretion exceeds the rate of glomerular filtration. Secretion in the principal cells of the late distal and cortical collecting tubules is a two step process, beginning with uptake from the interstitium into the cell by sodium potassium pump in the basal lateral cell membrane. Potassium then diffuses passively into the tubule fluid due to a concentration gradient created by sodium. Potassium diffusion occurs through renal outer medullary potassium channels and high conductance big potassium channels. The numbers of these channels are adjusted based on the need for potassium excretion. Therefore, potassium secretion by principal cells is controlled by three factors. The activity the sodium potassium pump. The electrochemical gradient from potassium secretion from the blood to the tubular lumen, and lastly the permeability of the tubular membrane from potassium. Control of potassium excretion occurs mainly as a result of the principal cells of the late distal and collecting tubules. The most important factors affecting secretion are extracellular potassium concentration, aldosterone, and tubular flow rate. Plasma potassium concentration is one of the most important mechanisms for regulating potassium secretion. Increased extracellular potassium concentration stimulates the sodium potassium pump, increasing uptake across the basal outer membrane. Of course, this increases the intracellular concentration of potassium in the principal cells, increasing the diffusion gradient. The same time, elevated potassium also stimulates synthesis of potassium channels and their translocation into the luminal membrane, allowing easier and more rapid diffusion. Lastly, the adrenal cortex is stimulated to release aldosterone. The astronaut stimulates active reabsorption of sodium ions by the principal cells of the light distal tubule and collecting ducts through the sodium potassium ATPase, of which of course transports sodium into the renal interstitial fluid and pumps potassium into the principal cells. Thus, aldosterone causes the reabsorption of sodium and the secretion of potassium. This is also important for sodium and water reabsorption, which we will go over more later. The astronaut also increases the number of potassium channels in the aluminum membrane and therefore permeability of potassium. You can see in the graph that increasing the plasma aldosterone concentration greatly increases urinary potassium excretion. AD Astra is a negative feedback control system in that aldosterone secretion is strongly controlled by extracellular potassium concentration. An increase in plasma potassium stimulates either strong secretion. In the absence of gastro secretion, such as Addison's disease, intracellular potassium concentration rises dangerously. Increase distal tubule flow rate. Can occur with volume expansion, high sodium intake, or some diuretics. Uh, some direct stimulate potassium secretion. This occurs through two main effects. Increased fluid delivery increases the net potassium secretion and also increases the number of high conduction back channels uh, in the tubular membranes, increasing the ACM diffusion. Tubular flow is important in preserving normal potassium excretion during fluctuations of high sodium intake. High sodium intake decreases aldosterone secretion, which should decrease secretion of potassium, but due to the high flow rate, potassium secretion is maintained. Therefore, I tubular rate and decrease thunderstorm secretion counterbalance each other. Hypocalcemia causes nerve and muscle excitability. In extreme cases, can cause hypocalcemia, whereas hypocalcemia depresses neuromuscular excitability and can lead to cardiac arrhythmias. Ionized calcium is the form, as that is biologically active at the cell membranes. About 50% of the calcium in the body is ionized. The other 40% is down to plasma proteins, and the last 10% is not ionized. Alkalosis causes greater plasma protein binding and therefore leads to hypercar can lead to hypocalcemia. Normally, uh, you can. Your intake is around 1000mg a day and about 900mg are excreted in the feces. Almost all calcium in the body is stored in the bones, with only 0.1% in extracellular fluid and 1% intracellular. The most important regulators of bone uptake and release are parathyroid hormone. We're definitely going to cover that in a future module as well. When hypercalcemia occurs, the parathyroid glands are stimulated to release parathyroid hormone, which acts to reabsorb bone, stimulates activation of vitamin D and increases renal tubular calcium reabsorption. Calcium is not secreted by the kidneys. Therefore, excretion is dependent about how much it's filtered into the renal tubules and how much is reabsorbed. Reabsorption of calcium occurs in the proximal tubule, the loop of hennelly, and in the distal tubule and the proximal tubule. Calcium is reabsorbed through the para cellular pathway, dissolved in water, as well as intracellular passive diffusion from tubular rumen and the calcium ATP and sodium calcium count of transporter in the basal lateral membrane. The loop of Henley and the distal tubule are affected by parathyroid hormone, which stimulates calcium reabsorption through cellular intracellular transport in the distal tubule. Reabsorption is almost entirely by active transport, utilizing the same mechanisms as the proximal tubule cells. Phosphate excretion is normally controlled primarily by an overflow mechanism. The transport maximum of five feet in renal tubules is 0.1 million miles a minute. And when less than this amount, it's filtered is all reabsorbed when there's more than this amount. Uh, GFR in excess is excreted due to large ingestions of phosphates in milk and meat phosphate. There's typically continual excretion of phosphate in the rock, promoting bone absorption. Parathyroid hormone also releases large amounts of phosphate and decreases sodium phosphate transporters. Thus, whenever parathyroid hormone is increased, more phosphate is excreted. Extracellular fluid volume is determined mainly by the balance between intake and output of water salt, which in most cases is determined by a person's habits and then regulated by the kidneys. This means the kidneys must adapt so their excretion matches intake. Sodium and water excretion are controlled by glomerular filtration and tubular reabsorption. They work in tandem and if one is changed without the other, the consequences could be catastrophic. Getting changes in sodium and fluid intake pressure not to resist and diuresis, help maintain fluid balance and minimize changes in blood volume, extracellular fluid volume, and arterial pressure. Increased fluid intake increases blood volume and therefore cardiac output. Blood pressure, which causes pressure diuresis and increased urinary output. An opposite sequence occurs when fluid intake decreases. Decreasing pressure decreases. Overall blood volume and extracellular fluid volume are usually controlled in parallel. When blood volume increases, it rapidly becomes distributed between interstitial spaces in the plasma. The factors that affect fluid movement into the interstitial spaces are the capillary hydrostatic pressure, the plasma colloid osmotic pressure. Capillary accountability in the lymphatic system. Any change in these factors can affect the amount of interstitial fluid. It should be noted that once blood volume rises 50% above normal, almost all additional fluid goes into the interstitial spaces and little remains in the blood. This means that the interstitial spaces act as an overflow reservoir for excess fluids. We will discuss the sympathetic nervous controlled renal excretion more thoroughly next semester. But this, uh, can serve as a brief introduction. The kidneys receive extensive sympathetic innervation, which causes constriction of renal arterials, leading to decreased GFR, increased tubular reabsorption of salt and water, rendered release, and increased angiotensin two in our dorsal. Angiotensin two. It's one of the body's most powerful controllers of sodium excretion. It decreases tubular reabsorption of sodium and water. Sodium intake and angiotensin two formation are closely linked. Increased sodium intake intake decreases angiotensin two formation. This is why Ace inhibitors have been shown to be extremely effective. Chronic blood pressure controls. Angiotensin two stimulates the secretion about DOS from, which in turn reduces sodium excretion. Huddlestone increases sodium reabsorption, especially in the collecting tubules and collecting ducts. Antidiuretic hormone allows the kidneys to form a small volume of concentrated urine while excreting normal amounts of salt. Water deprivation for 24 to 48 hours causes only a small decrease in extracellular fluid volume in arterial pressure. However, if ADHD blocked, this will cause a substantial fall in extracellular food volume and arterial pressure. AMP is released by cardiac atrial muscle fibers in response to stretch of the atria. It acts on kidneys, causing small increases in GFR, decreased red secretion, and decreased sodium reabsorption by the collecting ducts. Congestive heart failure can cause blood volume to increase 15 to 20% and extracellular fluid volume as much as 200% or more. Initially, there's reduced cardiac output and decreased ocular pressure, which activates sodium retention, especially the renin angiotensin aldosterone system. If the actual pressure does not return to normal, a positive feedback mechanism started. Kidneys continue to retain volume until circulatory congestion develops.